Search

Your search keyword '"O'Garra, A."' showing total 1,249 results
Start Over Author "O'Garra, A."
1,249 results on '"O'Garra, A."'

104. Blood transcriptomics reveal the evolution and resolution of the immune response in tuberculosis

Author

Tabone, Olivier, primary, Verma, Raman, additional, Singhania, Akul, additional, Chakravarty, Probir, additional, Branchett, William J., additional, Graham, Christine M., additional, Lee, Jo, additional, Trang, Tran, additional, Reynier, Frederic, additional, Leissner, Philippe, additional, Kaiser, Karine, additional, Rodrigue, Marc, additional, Woltmann, Gerrit, additional, Haldar, Pranabashis, additional, and O’Garra, Anne, additional

Published
2021
Full Text
View/download PDF

105. Clinical outcomes of COVID-19 in long-term care facilities for people with epilepsy

Author

Simona Balestrini, Matthias J. Koepp, Sonia Gandhi, Hannah M. Rickman, Gee Yen Shin, Catherine F. Houlihan, Jonny Anders-Cannon, Katri Silvennoinen, Fenglai Xiao, Sara Zagaglia, Kirsty Hudgell, Mariusz Ziomek, Paul Haimes, Adam Sampson, Annie Parker, J. Helen Cross, Rosemarie Pardington, Eleni Nastouli, Charles Swanton, Josemir W. Sander, Sanjay M. Sisodiya, Jim Aitken, Zoe Allen, Rachel Ambler, Karen Ambrose, Emma Ashton, Alida Avola, Samutheswari Balakrishnan, Caitlin Barns-Jenkins, Genevieve Barr, Sam Barrell, Souradeep Basu, Rupert Beale, Clare Beesley, Nisha Bhardwaj, Shahnaz Bibi, Ganka Bineva-Todd, Dhruva Biswas, Michael J. Blackman, Dominique Bonnet, Faye Bowker, Malgorzata Broncel, Claire Brooks, Michael D. Buck, Andrew Buckton, Timothy Budd, Alana Burrell, Louise Busby, Claudio Bussi, Simon Butterworth, Matthew Byott, Fiona Byrne, Richard Byrne, Simon Caidan, Joanna Campbell, Johnathan Canton, Ana Cardoso, Nick Carter, Luiz Carvalho, Raffaella Carzaniga, Natalie Chandler, Qu Chen, Peter Cherepanov, Laura Churchward, Graham Clark, Bobbi Clayton, Clementina Cobolli Gigli, Zena Collins, Sally Cottrell, Margaret Crawford, Laura Cubitt, Tom Cullup, Heledd Davies, Patrick Davis, Dara Davison, Vicky Dearing, Solene Debaisieux, Monica Diaz-Romero, Alison Dibbs, Jessica Diring, Paul C. Driscoll, Annalisa D'Avola, Christopher Earl, Amelia Edwards, Chris Ekin, Dimitrios Evangelopoulos, Rupert Faraway, Antony Fearns, Aaron Ferron, Efthymios Fidanis, Dan Fitz, James Fleming, Daniel Frampton, Bruno Frederico, Alessandra Gaiba, Anthony Gait, Steve Gamblin, Kathleen Gärtner, Liam Gaul, Helen M. Golding, Jacki Goldman, Robert Goldstone, Belen Gomez Dominguez, Hui Gong, Paul R. Grant, Maria Greco, Mariana Grobler, Anabel Guedan, Maximiliano G. Gutierrez, Fiona Hackett, Ross Hall, Steinar Halldorsson, Suzanne Harris, Sugera Hashim, Emine Hatipoglu, Lyn Healy, Judith Heaney, Susanne Herbst, Graeme Hewitt, Theresa Higgins, Steve Hindmarsh, Rajnika Hirani, Joshua Hope, Elizabeth Horton, Beth Hoskins, Michael Howell, Louise Howitt, Jacqueline Hoyle, Mint R. Htun, Michael Hubank, Hector Huerga Encabo, Deborah Hughes, Jane Hughes, Almaz Huseynova, Ming-Shih Hwang, Rachael Instrell, Deborah Jackson, Mariam Jamal-Hanjani, Lucy Jenkins, Ming Jiang, Mark Johnson, Leigh Jones, Nnennaya Kanu, George Kassiotis, Gavin Kelly, Louise Kiely, Anastacio King Spert Teixeira, Stuart Kirk, Svend Kjaer, Ellen Knuepfer, Nikita Komarov, Paul Kotzampaltiris, Konstantinos Kousis, Tammy Krylova, Ania Kucharska, Robyn Labrum, Catherine Lambe, Michelle Lappin, Stacey-Ann Lee, Andrew Levett, Lisa Levett, Marcel Levi, Hon Wing Liu, Sam Loughlin, Wei-Ting Lu, James I. MacRae, Akshay Madoo, Julie A. Marczak, Mimmi Martensson, Thomas Martinez, Bishara Marzook, John Matthews, Joachim M. Matz, Samuel McCall, Laura E. McCoy, Fiona McKay, Edel C. McNamara, Carlos M. Minutti, Gita Mistry, Miriam Molina-Arcas, Beatriz Montaner, Kylie Montgomery, Catherine Moore, David Moore, Anastasia Moraiti, Lucia Moreira-Teixeira, Joyita Mukherjee, Cristina Naceur-Lombardelli, Aileen Nelson, Jerome Nicod, Luke Nightingale, Stephanie Nofal, Paul Nurse, Savita Nutan, Caroline Oedekoven, Anne O'Garra, Jean D. O'Leary, Jessica Olsen, Olga O'Neill, Nicola O'Reilly, Paula Ordonez Suarez, Neil Osborne, Amar Pabari, Aleksandra Pajak, Venizelos Papayannopoulos, Stavroula M Paraskevopoulou, Namita Patel, Yogen Patel, Oana Paun, Nigel Peat, Laura Peces-Barba Castano, Ana Perez Caballero, Jimena Perez-Lloret, Magali S. Perrault, Abigail Perrin, Roy Poh, Enzo Z. Poirier, James M. Polke, Marc Pollitt, Lucia Prieto-Godino, Alize Proust, Clinda Puvirajasinghe, Christophe Queval, Vijaya Ramachandran, Abhinay Ramaprasad, Peter Ratcliffe, Laura Reed, Caetano Reis e Sousa, Kayleigh Richardson, Sophie Ridewood, Fiona Roberts, Rowenna Roberts, Angela Rodgers, Pablo Romero Clavijo, Annachiara Rosa, Alice Rossi, Chloe Roustan, Andrew Rowan, Erik Sahai, Aaron Sait, Katarzyna Sala, Emilie Sanchez, Theo Sanderson, Pierre Santucci, Fatima Sardar, Adam Sateriale, Jill A. Saunders, Chelsea Sawyer, Anja Schlott, Edina Schweighoffer, Sandra Segura-Bayona, Rajvee Shah Punatar, Maryam Shahmanesh, Joe Shaw, Mariana Silva Dos Santos, Margaux Silvestre, Matthew Singer, Daniel M. Snell, Ok-Ryul Song, Moira J. Spyer, Louisa Steel, Amy Strange, Adrienne E. Sullivan, Michele S.Y. Tan, Zoe H. Tautz-Davis, Effie Taylor, Gunes Taylor, Harriet B. Taylor, Alison Taylor-Beadling, Fernanda Teixeira Subtil, Berta Terré Torras, Patrick Toolan-Kerr, Francesca Torelli, Tea Toteva, Moritz Treeck, Hadija Trojer, Ming-Han C. Tsai, James M.A. Turner, Melanie Turner, Jernej Ule, Rachel Ulferts, Sharon P. Vanloo, Selvaraju Veeriah, Subramanian Venkatesan, Karen Vousden, Andreas Wack, Claire Walder, Philip A. Walker, Yiran Wang, Sophia Ward, Catharina Wenman, Luke Williams, Matthew J. Williams, Wai Keong Wong, Joshua Wright, Mary Wu, Lauren Wynne, Zheng Xiang, Melvyn Yap, Julian A. Zagalak, Davide Zecchin, Rachel Zillwood, Santhakumari Carthiyaniamma, Jane DeTisi, Julie Dick, Andrea Hill, Karin Kipper, Birinder Kullar, Sarah Norris, Fergus Rugg-Gunn, Rebecca Salvatierra, Gabriel Shaya, Astrid Sloan, Priyanka Singh, James Varley, Ben Whatley, and Academic Medical Center

Subjects
Male, Pediatrics, CCC, Crick COVID Consortium, SWGC, Sir William Gowers Centre, Comorbidity, Residential Facilities, Cohort Studies, Behavioral Neuroscience, Epilepsy, 0302 clinical medicine, Case fatality rate, Infection control, 030212 general & internal medicine, Care Models, COVID-19, coronavirus disease 2019, Aged, 80 and over, Surveillance, Middle Aged, 3. Good health, Treatment Outcome, Neurology, UCLH, University College London Hospitals NHS Foundation Trust, PEG, percutaneous endoscopic gastrostomy, STE, St Elizabeth’s Centre, Female, medicine.symptom, PPE, personal protective equipment, Cohort study, Adult, medicine.medical_specialty, Isolation (health care), Clinical Neurology, Asymptomatic, Article, Young Adult, 03 medical and health sciences, medicine, Humans, YE, Young Epilepsy, Aged, SARS-CoV-2, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Infection Control, business.industry, SARS-CoV-2, Prevention, Vulnerable people, COVID-19, TM, The Meath, medicine.disease, Long-Term Care, CCE, Chalfont Centre for Epilepsy, United Kingdom, Long-term care, Neurology (clinical), business, 030217 neurology & neurosurgery, Contact tracing
Abstract

Highlights • We found a high asymptomatic rate in vulnerable people with epilepsy. • Enhanced surveillance allows to quickly contain outbreaks. • We report a low rate of COVID-19 morbidity and mortality in a long-term care facility. • Preventative measures allow reducing resident-to-resident and -to-caregiver transmission. • Children and young adults appear to have lower infection rates., In this cohort study, we aim to compare outcomes from coronavirus disease 2019 (COVID-19) in people with severe epilepsy and other co-morbidities living in long-term care facilities which all implemented early preventative measures, but different levels of surveillance. During 25-week observation period (16 March–6 September 2020), we included 404 residents (118 children), and 1643 caregivers. We compare strategies for infection prevention, control, and containment, and related outcomes, across four UK long-term care facilities. Strategies included early on-site enhancement of preventative and infection control measures, early identification and isolation of symptomatic cases, contact tracing, mass surveillance of asymptomatic cases and contacts. We measured infection rate among vulnerable people living in the facilities and their caregivers, with asymptomatic and symptomatic cases, including fatality rate. We report 38 individuals (17 residents) who tested severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive, with outbreaks amongst residents in two facilities. At Chalfont Centre for Epilepsy (CCE), 10/98 residents tested positive: two symptomatic (one died), eight asymptomatic on weekly enhanced surveillance; 2/275 caregivers tested positive: one symptomatic, one asymptomatic. At St Elizabeth’s (STE), 7/146 residents tested positive: four symptomatic (one died), one positive during hospital admission for symptoms unrelated to COVID-19, two asymptomatic on one-off testing of all 146 residents; 106/601 symptomatic caregivers were tested, 13 positive. In addition, during two cycles of systematically testing all asymptomatic carers, four tested positive. At The Meath (TM), 8/80 residents were symptomatic but none tested; 26/250 caregivers were tested, two positive. At Young Epilepsy (YE), 8/80 children were tested, all negative; 22/517 caregivers were tested, one positive. Infection outbreaks in long-term care facilities for vulnerable people with epilepsy can be quickly contained, but only if asymptomatic individuals are identified through enhanced surveillance at resident and caregiver level. We observed a low rate of morbidity and mortality, which confirmed that preventative measures with isolation of suspected and confirmed COVID-19 residents can reduce resident-to-resident and resident-to-caregiver transmission. Children and young adults appear to have lower infection rates. Even in people with epilepsy and multiple co-morbidities, we observed a high percentage of asymptomatic people suggesting that epilepsy-related factors (anti-seizure medications and seizures) do not necessarily lead to poor outcomes.

Published
2021

108. Impact of gameplay vs. reading on mental models of social-ecological systems

Author

Diana Reckien, Grace H. Bachman, Joey J. Lee, Tanya O'Garra, Stephanie Pfirman, Elizabeth Bachrach Simon, Jessica Brunacini, UT-I-ITC-PLUS, Faculty of Geo-Information Science and Earth Observation, and Department of Urban and Regional Planning and Geo-Information Management

Subjects
serious games, fuzzy cognitive mapping, Ecology, QH301-705.5, media_common.quotation_subject, Complex system, systems thinking, Informal education, Ecological systems theory, Variety (cybernetics), climate change, Dynamics (music), Intervention (counseling), Reading (process), ITC-ISI-JOURNAL-ARTICLE, arctic, polar regions, Systems thinking, Biology (General), Psychology, ITC-GOLD, QH540-549.5, media_common, Cognitive psychology
Abstract

Climate change is a highly complex social-ecological problem characterized by system-type dynamics that are important to communicate in a variety of settings, ranging from formal education to decision makers to informal education of the general public. Educational games are one approach that may enhance systems thinking skills. This study used a randomized controlled experiment to compare the impact on the mental models of participants of an educational card game vs. an illustrated article about the Arctic social-ecological system. A total of 41 participants (game: n = 20; reading: n = 21) created pre- and post-intervention mental models of the system, based on a "fuzzy cognitive mapping" approach. Maps were analyzed using network statistics. Both reading the article and playing the game resulted in measurable increases in systems understanding. The group reading the article perceived a more complex system after the intervention, with overall learning gains approximately twice those of the game players. However, game players demonstrated similar learning gains as article readers regarding the climate system, actions both causing environmental problems and protecting the Arctic, as well as the importance of the base- and mid-levels of the food chain. These findings contribute to the growing evidence showing that games are important resources to include as strategies for building capacity to understand and steward sustainable social-ecological systems, in both formal and informal education.

Published
2021
Full Text
View/download PDF

109. Blood transcriptomics reveal the evolution and resolution of the immune response in tuberculosis

Author

Jo Lee, Olivier Tabone, Raman Verma, Christine M. Graham, William J Branchett, Philippe Leissner, Tran Trang, Frédéric Reynier, Anne O'Garra, Pranabashis Haldar, Probir Chakravarty, Gerrit Woltmann, Akul Singhania, Marc Rodrigue, and Karine Kaiser

Subjects
Male, Model organisms, Treatment response, Tuberculosis, Immunology, Antitubercular Agents, Gene Expression, Infectious Disease, Disease, Article, Transcriptome, Infectious Disease and Host Defense, Immune system, Risk Factors, Active tb, Immunology and Allergy, Medicine, Humans, Prospective Studies, Tuberculosis, Pulmonary, Subclinical infection, Computational & Systems Biology, Chemical Biology & High Throughput, Human Biology & Physiology, business.industry, Sequence Analysis, RNA, FOS: Clinical medicine, Genome Integrity & Repair, Tumour Biology, medicine.disease, Biological Evolution, Treatment Outcome, Cohort, Female, Contact Tracing, business, Genetics & Genomics
Abstract

TB results in 1.5 million deaths per year, yet a low percentage of M. tuberculosis–infected individuals progress to TB. Knowledge of the early immune response during TB progression and on treatment will inform clinical management of the disease., Blood transcriptomics have revealed major characteristics of the immune response in active TB, but the signature early after infection is unknown. In a unique clinically and temporally well-defined cohort of household contacts of active TB patients that progressed to TB, we define minimal changes in gene expression in incipient TB increasing in subclinical and clinical TB. While increasing with time, changes in gene expression were highest at 30 d before diagnosis, with heterogeneity in the response in household TB contacts and in a published cohort of TB progressors as they progressed to TB, at a bulk cohort level and in individual progressors. Blood signatures from patients before and during anti-TB treatment robustly monitored the treatment response distinguishing early and late responders. Blood transcriptomics thus reveal the evolution and resolution of the immune response in TB, which may help in clinical management of the disease.

Published
2021
Full Text
View/download PDF

110. An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis

Author

Berry, Matthew P.R., Graham, Christine M., McNab, Finlay W., Xu, Zhaohui, Bloch, Susannah A.A., Oni, Tolu, Wilkinson, Katalin A., Banchereau, Romain, Skinner, Jason, Wilkinson, Robert J., Quinn, Charles, Blankenship, Derek, Dhawan, Ranju, Cush, John J., Mejias, Asuncion, Ramilo, Octavio, Kon, Onn M., Pascua, Virginia, Banchereau, Jacques, Chaussabel, Damien, and O'Garra, Anne

Subjects
Interferon -- Research -- Analysis, Gene expression -- Research -- Analysis -- Genetic aspects, Immune response -- Analysis -- Research, Tuberculosis -- Genetic aspects -- Development and progression -- Research
Abstract

Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis, is a major cause of morbidity and mortality worldwide. Efforts to control it are hampered by difficulties with diagnosis, prevention and treatment (1,2). Most people infected with M. tuberculosis remain asymptomatic, termed latent TB, with a 10% lifetime risk of developing active TB disease. Current tests, however, cannot identify which individuals will develop disease (3). The immune response to M. tuberculosis is complex and incompletely characterized, hindering development of new diagnostics, therapies and vaccines (4,5). Here we identify a whole-blood 393 transcript signature for active TB in intermediate and high-burden settings, correlating with radiological extent of disease and reverting to that of healthy controls after treatment. A subset of patients with latent TB had signatures similar to those in patients with active TB. We also identify a specific 86-transcript signature that discriminates active TB from other inflammatory and infectious diseases. Modular and pathway analysis revealed that the TB signature was dominated by a neutrophil-driven interferon (IFN)inducible gene profile, consisting of both IFN-γ and type I IFN-αβ signalling. Comparison with transcriptional signatures in purified cells and flow cytometric analysis suggest that this TB signature reflects changes in cellular composition and altered gene expression. Although an IFN-inducible signature was also observed in whole blood of patients with systemic lupus erythematosus (SLE), their complete modular signature differed from TB, with increased abundance of plasma cell transcripts. Our studies demonstrate a hitherto underappreciated role of type I IFN-αβ signalling in the pathogenesis of TB, which has implications for vaccine and therapeutic development. Our study also provides a broad range of transcriptional biomarkers with potential as diagnostic and prognostic tools to combat the TB epidemic., Blood transcriptional profiling has improved diagnosis and understanding of disease pathogenesis (6-9). Such a comprehensive unbiased survey will provide insights into the immunopathogenesis of TB, leading to advances in control [...]

Published
2010
Full Text
View/download PDF

112. Correction: Transcriptional Blood Signatures Distinguish Pulmonary Tuberculosis, Pulmonary Sarcoidosis, Pneumonias and Lung Cancers.

Author

Chloe I. Bloom, Christine M. Graham, Matthew P. R. Berry, Fotini Rozakeas, Paul S. Redford, Yuanyuan Wang, Zhaohui Xu, Katalin A. Wilkinson, Robert J. Wilkinson, Yvonne Kendrick, Gilles Devouassoux, Tristan Ferry, Makoto Miyara, Diane Bouvry, Valeyre Dominique, Guy Gorochov, Derek Blankenship, Mitra Saadatian, Phillip Vanhems, Huw Beynon, Rama Vancheeswaran, Melissa Wickremasinghe, Damien Chaussabel, Jacques Banchereau, Virginia Pascual, Ling-pei Ho, Marc Lipman, and Anne O’Garra

Subjects
Medicine, Science
Published
2013
Full Text
View/download PDF

113. Transcriptional blood signatures distinguish pulmonary tuberculosis, pulmonary sarcoidosis, pneumonias and lung cancers.

Author

Chloe I Bloom, Christine M Graham, Matthew P R Berry, Fotini Rozakeas, Paul S Redford, Yuanyuan Wang, Zhaohui Xu, Katalin A Wilkinson, Robert J Wilkinson, Yvonne Kendrick, Gilles Devouassoux, Tristan Ferry, Makoto Miyara, Diane Bouvry, Dominique Valeyre, Guy Gorochov, Derek Blankenship, Mitra Saadatian, Phillip Vanhems, Huw Beynon, Rama Vancheeswaran, Melissa Wickremasinghe, Damien Chaussabel, Jacques Banchereau, Virginia Pascual, Ling-Pei Ho, Marc Lipman, and Anne O'Garra

Subjects
Medicine, Science
Abstract

New approaches to define factors underlying the immunopathogenesis of pulmonary diseases including sarcoidosis and tuberculosis are needed to develop new treatments and biomarkers. Comparing the blood transcriptional response of tuberculosis to other similar pulmonary diseases will advance knowledge of disease pathways and help distinguish diseases with similar clinical presentations.To determine the factors underlying the immunopathogenesis of the granulomatous diseases, sarcoidosis and tuberculosis, by comparing the blood transcriptional responses in these and other pulmonary diseases.We compared whole blood genome-wide transcriptional profiles in pulmonary sarcoidosis, pulmonary tuberculosis, to community acquired pneumonia and primary lung cancer and healthy controls, before and after treatment, and in purified leucocyte populations.An Interferon-inducible neutrophil-driven blood transcriptional signature was present in both sarcoidosis and tuberculosis, with a higher abundance and expression in tuberculosis. Heterogeneity of the sarcoidosis signature correlated significantly with disease activity. Transcriptional profiles in pneumonia and lung cancer revealed an over-abundance of inflammatory transcripts. After successful treatment the transcriptional activity in tuberculosis and pneumonia patients was significantly reduced. However the glucocorticoid-responsive sarcoidosis patients showed a significant increase in transcriptional activity. 144-blood transcripts were able to distinguish tuberculosis from other lung diseases and controls.Tuberculosis and sarcoidosis revealed similar blood transcriptional profiles, dominated by interferon-inducible transcripts, while pneumonia and lung cancer showed distinct signatures, dominated by inflammatory genes. There were also significant differences between tuberculosis and sarcoidosis in the degree of their transcriptional activity, the heterogeneity of their profiles and their transcriptional response to treatment.

Published
2013
Full Text
View/download PDF

114. Biology and therapeutic potential of interleukin-10

Author

Anne O'Garra, Paulo Vieira, Margarida Saraiva, Instituto de Investigação e Inovação em Saúde (I3S), Universidade do Porto = University of Porto, Lymphopoïèse (Lymphopoïèse (UMR_1223 / U1223 / U-Pasteur_4)), Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cellule Pasteur, Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, The Francis Crick Institute [London], Imperial College London, M. Saraiva is financed by Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020 Operational Program for Competitiveness and Internationalisation, Portugal 2020, and by Portuguese funds through Fundação para a Ciência e Tecnologia in the framework of the project ‘‘Institute for Research and Innovation in Health Sciences’’ (POCI-01-0145-FEDER-007274), and by Fundação para a Ciência e Tecnologia through Estimulo Individual ao Emprego Científico. P. Vieira is funded by Agence National de la Recherche, through the project MYELOTEN (ANR-13-ISV1-0003-01), and by the Institut Pasteur, France. A. O’Garra is funded by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001126), the UK Medical Research Council (FC001126), and the Wellcome Trust (FC001126), ANR-13-ISV1-0003,MYELOTEN,DEREGULATION DE L'HEMATOPOIESE PAR LA SUREXPRESSION DE L'INTERLEUKINE-10 : IMPLICATIONS DANS LE DEVELOPPEMENT DE PATHOLOGIES HEMATOLOGIQUES(2013), Universidade do Porto [Porto], Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), PRES Sorbonne Paris Cité-Université Paris Diderot - Paris 7 (UPD7), The Francis Crick Institute, and Universidade do Porto

Subjects
medicine.medical_treatment, Immunology, Reviews, Adipose tissue, Autoimmunity, Context (language use), Review, Biology, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Mediator, Neoplasms, medicine, Animals, Humans, Immunology and Allergy, Cytotoxic T cell, 030304 developmental biology, Inflammation, 0303 health sciences, Interleukin-10, 3. Good health, Interleukin 10, Cytokine, Cytokines, [SDV.IMM]Life Sciences [q-bio]/Immunology, Wound healing, Neuroscience, 030215 immunology
Abstract

The authors review the molecular mechanisms regulating IL-10 production and response and describe classic and novel functions of IL-10 in immune and non-immune cells. They further discuss the therapeutic potential of IL-10 in different diseases and the outstanding questions underlying an effective application of IL-10 in clinical settings., The cytokine IL-10 is a key anti-inflammatory mediator ensuring protection of a host from over-exuberant responses to pathogens and microbiota, while playing important roles in other settings as sterile wound healing, autoimmunity, cancer, and homeostasis. Here we discuss our current understanding of the regulation of IL-10 production and of the molecular pathways associated with IL-10 responses. In addition to IL-10’s classic inhibitory effects on myeloid cells, we also describe the nonclassic roles attributed to this pleiotropic cytokine, including how IL-10 regulates basic processes of neural and adipose cells and how it promotes CD8 T cell activation, as well as epithelial repair. We further discuss its therapeutic potential in the context of different diseases and the outstanding questions that may help develop an effective application of IL-10 in diverse clinical settings.

Published
2019
Full Text
View/download PDF

116. JEM women in STEM: Unique journeys with a common purpose

Author

Anne O'Garra, Arlene H. Sharpe, Sara Cherry, Emmanuelle Passegué, Yasmine Belkaid, and Susan M. Kaech

Subjects
0301 basic medicine, media_common.quotation_subject, education, Immunology, MEDLINE, Face (sociological concept), 03 medical and health sciences, Viewpoint, 0302 clinical medicine, Medical Laboratory Personnel, ComputingMilieux_COMPUTERSANDEDUCATION, Immunology and Allergy, Humans, Sociology, health care economics and organizations, media_common, ComputingMilieux_THECOMPUTINGPROFESSION, Life events, Gender studies, humanities, ComputingMilieux_GENERAL, 030104 developmental biology, Women in science, Female, 030215 immunology, Diversity (politics)
Abstract

Academic Editors at JEM share their experiences of being women in STEM and suggest future directions to support the career of female scientists., Before one can think of the challenges that face women in science and the hurdles that impair their development into leadership positions, it is worth considering the diversity within the collective of women scientists at the level of culture and past experience and life events.

Published
2020

117. Development of a Fixed Repertoire of Blood Transcriptome Modules Based on Co-expression Patterns Across Immunological States

Author

Matthew Altman, Darawan Rinchai, Nicole Baldwin, Mohammed Toufiq, Elizabeth Whalen, Mathieu Garand, Basirudeen Kabeer, Mohamed Alfaki, Scott Presnell, Prasong Khaenam, Aaron Ayllon-Benitez, Fleur Mougin, Patricia Thébault, Laurent chiche, Noemie Jourde-Chiche, Theodore Phillips, Goran Klintmalm, Anne O'Garra, Matthew Berry, Chloe Bloom, Robert Wilkinson, Christine Graham, Marc Lipman, Ganjana Lertmemongkolchai, Davide Bedognetti, Rodolphe Thiébaut, Farrah Kheradmand, Asuncion Mejias, Octavio Ramilo, Karolina Palucka, Virginia Pascual, Jacques Banchereau, and Damien Chaussabel

Abstract

As the capacity for generating large scale data continues to grow the ability to extract meaningful biological knowledge from it remains a limitation. Here we describe the development of a new fixed repertoire of transcriptional modules. It is meant to serve as a stable reusable framework for the analysis and interpretation of blood transcriptome profiling data. It is supported by customized resources, which include analysis workflows, fingerprint grid plots data visualizations, interactive web applications. These provide access to a vast number of module-specific functional profiling reports, reference transcriptional profiles, and give users the ability to visualize changes in transcript abundance across the modular repertoire at different granularity levels. A use case focusing on a set of six modules comprising interferon-inducible genes is also provided. Taken together, this well-characterized set of modules may be employed for the interpretation and benchmarking of blood transcriptome profiles obtained within and across patient cohorts.

Published
2020
Full Text
View/download PDF

118. Pandemic peak SARS-CoV-2 infection and seroconversion rates in London frontline health-care workers

Author

Catherine F Houlihan, Nina Vora, Thomas Byrne, Dan Lewer, Gavin Kelly, Judith Heaney, Sonia Gandhi, Moira J Spyer, Rupert Beale, Peter Cherepanov, David Moore, Richard Gilson, Steve Gamblin, George Kassiotis, Laura E McCoy, Charles Swanton, Andrew Hayward, Eleni Nastouli, Jim Aitken, Zoe Allen, Rachel Ambler, Karen Ambrose, Emma Ashton, Alida Avola, Samutheswari Balakrishnan, Caitlin Barns-Jenkins, Genevieve Barr, Sam Barrell, Souradeep Basu, Clare Beesley, Nisha Bhardwaj, Shahnaz Bibi, Ganka Bineva-Todd, Dhruva Biswas, Michael J Blackman, Dominique Bonnet, Faye Bowker, Malgorzata Broncel, Claire Brooks, Michael D Buck, Andrew Buckton, Timothy Budd, Alana Burrell, Louise Busby, Claudio Bussi, Simon Butterworth, Fiona Byrne, Richard Byrne, Simon Caidan, Joanna Campbell, Johnathan Canton, Ana Cardoso, Nick Carter, Luiz Carvalho, Raffaella Carzaniga, Natalie Chandler, Qu Chen, Laura Churchward, Graham Clark, Bobbi Clayton, Clementina Cobolli Gigli, Zena Collins, Sally Cottrell, Margaret Crawford, Laura Cubitt, Tom Cullup, Heledd Davies, Patrick Davis, Dara Davison, Annalisa D'Avola, Vicky Dearing, Solene Debaisieux, Monica Diaz-Romero, Alison Dibbs, Jessica Diring, Paul C Driscoll, Christopher Earl, Amelia Edwards, Chris Ekin, Dimitrios Evangelopoulos, Rupert Faraway, Antony Fearns, Aaron Ferron, Efthymios Fidanis, Dan Fitz, James Fleming, Bruno Frederico, Alessandra Gaiba, Anthony Gait, Liam Gaul, Helen M Golding, Jacki Goldman, Robert Goldstone, Belen Gomez Dominguez, Hui Gong, Paul R Grant, Maria Greco, Mariana Grobler, Anabel Guedan, Maximiliano G Gutierrez, Fiona Hackett, Ross Hall, Steinar Halldorsson, Suzanne Harris, Sugera Hashim, Lyn Healy, Susanne Herbst, Graeme Hewitt, Theresa Higgins, Steve Hindmarsh, Rajnika Hirani, Joshua Hope, Elizabeth Horton, Beth Hoskins, Michael Howell, Louise Howitt, Jacqueline Hoyle, Mint R Htun, Michael Hubank, Hector Huerga Encabo, Deborah Hughes, Jane Hughes, Almaz Huseynova, Ming-Shih Hwang, Rachael Instrell, Deborah Jackson, Mariam Jamal-Hanjani, Lucy Jenkins, Ming Jiang, Mark Johnson, Leigh Jones, Nnennaya Kanu, Louise Kiely, Anastacio King Spert Teixeira, Stuart Kirk, Svend Kjaer, Ellen Knuepfer, Nikita Komarov, Paul Kotzampaltiris, Konstantinos Kousis, Tammy Krylova, Ania Kucharska, Robyn Labrum, Catherine Lambe, Michelle Lappin, Stacey-Ann Lee, Andrew Levett, Lisa Levett, Marcel Levi, Hon-Wing Liu, Sam Loughlin, Wei-Ting Lu, James I MacRae, Akshay Madoo, Julie A Marczak, Mimmi Martensson, Thomas Martinez, Bishara Marzook, John Matthews, Joachim M Matz, Samuel McCall, Fiona McKay, Edel C McNamara, Carlos M Minutti, Gita Mistry, Miriam Molina-Arcas, Beatriz Montaner, Kylie Montgomery, Catherine Moore, Anastasia Moraiti, Lucia Moreira-Teixeira, Joyita Mukherjee, Cristina Naceur-Lombardelli, Aileen Nelson, Jerome Nicod, Luke Nightingale, Stephanie Nofal, Paul Nurse, Savita Nutan, Caroline Oedekoven, Anne O'Garra, Jean D O'Leary, Jessica Olsen, Olga O'Neill, Paula Ordonez Suarez, Nicola O'Reilly, Neil Osborne, Amar Pabari, Aleksandra Pajak, Venizelos Papayannopoulos, Namita Patel, Yogen Patel, Oana Paun, Nigel Peat, Laura Peces-Barba Castano, Ana Perez Caballero, Jimena Perez-Lloret, Magali S Perrault, Abigail Perrin, Roy Poh, Enzo Z Poirier, James M Polke, Marc Pollitt, Lucia Prieto-Godino, Alize Proust, Rajvee Shah Punatar, Clinda Puvirajasinghe, Christophe Queval, Vijaya Ramachandran, Abhinay Ramaprasad, Peter Ratcliffe, Laura Reed, Caetano Reis e Sousa, Kayleigh Richardson, Sophie Ridewood, Rowenna Roberts, Angela Rodgers, Pablo Romero Clavijo, Annachiara Rosa, Alice Rossi, Chloe Roustan, Andrew Rowan, Erik Sahai, Aaron Sait, Katarzyna Sala, Theo Sanderson, Pierre Santucci, Fatima Sardar, Adam Sateriale, Jill A Saunders, Chelsea Sawyer, Anja Schlott, Edina Schweighoffer, Sandra Segura-Bayona, Joe Shaw, Gee Yen Shin, Mariana Silva Dos Santos, Margaux Silvestre, Matthew Singer, Daniel M Snell, Ok-Ryul Song, Louisa Steel, Amy Strange, Adrienne E Sullivan, Michele SY Tan, Zoe H Tautz-Davis, Effie Taylor, Gunes Taylor, Harriet B Taylor, Alison Taylor-Beadling, Fernanda Teixeira Subtil, Berta Terré Torras, Patrick Toolan-Kerr, Francesca Torelli, Tea Toteva, Moritz Treeck, Hadija Trojer, Ming-Han C Tsai, James MA Turner, Melanie Turner, Jernej Ule, Rachel Ulferts, Sharon P Vanloo, Selvaraju Veeriah, Subramanian Venkatesan, Karen Vousden, Andreas Wack, Claire Walder, Philip A Walker, Yiran Wang, Sophia Ward, Catharina Wenman, Luke Wiliams, Matthew J Williams, Wai Keong Wong, Joshua Wright, Mary Wu, Lauren Wynne, Zheng Xiang, Melvyn Yap, Julian A Zagalak, Davide Zecchin, Rachel Zillwood, Rebecca Matthews, Abigail Severn, Sajida Adam, Louise Enfield, Angela McBride, Kathleen Gärtner, Sarah Edwards, Fabiana Lorencatto, Susan Michie, Ed Manley, Maryam Shahmanesh, Hinal Lukha, Paulina Prymas, Hazel McBain, Robert Shortman, Leigh Wood, Claudia Davies, Bethany Williams, Kevin W Ng, Georgina H Cornish, Nikhil Faulkner, Andrew Riddell, Philip Hobson, Ana Agua-Doce, Kerol Bartolovic, Emma Russell, Lotte Carr, Emilie Sanchez, Daniel Frampton, Matthew Byott, Stavroula M Paraskevopoulou, Elise Crayton, Carly Meyer, Triantafylia Gkouleli, Andrea Stoltenberg, Veronica Ranieri, Tom Byrne, Fiona Roberts, and Emine Hatipoglu

Subjects
Adult, 2019-20 coronavirus outbreak, Infectious Disease Transmission, Patient-to-Professional, Coronavirus disease 2019 (COVID-19), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Health Personnel, Pneumonia, Viral, Viral transmission, Antibodies, Viral, Risk Assessment, Article, Betacoronavirus, Environmental health, Occupational Exposure, Pandemic, Health care, London, Medicine, Humans, Prospective Studies, Seroconversion, Pandemics, Cross Infection, business.industry, SARS-CoV-2, COVID-19, General Medicine, Occupational exposure, business, Coronavirus Infections
Published
2020

119. Scalable and robust SARS-CoV-2 testing in an academic center

Author

Aitken, Jim, Ambrose, Karen, Barrell, Sam, Beale, Rupert, Bineva-Todd, Ganka, Biswas, Dhruva, Byrne, Richard, Caidan, Simon, Cherepanov, Peter, Churchward, Laura, Clark, Graham, Crawford, Margaret, Cubitt, Laura, Dearing, Vicky, Earl, Christopher, Edwards, Amelia, Ekin, Chris, Fidanis, Efthymios, Gaiba, Alessandra, Gamblin, Steve, Gandhi, Sonia, Goldman, Jacki, Goldstone, Robert, Grant, Paul R., Greco, Maria, Heaney, Judith, Hindmarsh, Steve, Houlihan, Catherine F., Howell, Michael, Hubank, Michael, Hughes, Deborah, Instrell, Rachael, Jackson, Deborah, Jamal-Hanjani, Mariam, Jiang, Ming, Johnson, Mark, Jones, Leigh, Kanu, Nnennaya, Kassiotis, George, Kirk, Stuart, Kjaer, Svend, Levett, Andrew, Levett, Lisa, Levi, Marcel, Lu, Wei-Ting, MacRae, James I., Matthews, John, McCoy, Laura E., Moore, Catherine, Moore, David, Nastouli, Eleni, Nicod, Jerome, Nightingale, Luke, Olsen, Jessica, O’Reilly, Nicola, Pabari, Amar, Papayannopoulos, Venizelos, Patel, Namita, Peat, Nigel, Pollitt, Marc, Ratcliffe, Peter, Reis e Sousa, Caetano, Rosa, Annachiara, Rosenthal, Rachel, Roustan, Chloe, Rowan, Andrew, Shin, Gee Yen, Snell, Daniel M., Song, Ok-Ryul, Spyer, Moira J., Strange, Amy, Swanton, Charles, Turner, James M. A., Turner, Melanie, Wack, Andreas, Walker, Philip A., Ward, Sophia, Wong, Wai Keong, Wright, Joshua, Wu, Mary, Allen, Zoe, Ambler, Rachel, Ashton, Emma, Avola, Alida, Balakrishnan, Samutheswari, Barns-Jenkins, Caitlin, Barr, Genevieve, Basu, Souradeep, Beesley, Clare, Bhardwaj, Nisha, Bibi, Shahnaz, Blackman, Michael J., Bonnet, Dominique, Bowker, Faye, Broncel, Malgorzata, Brooks, Claire, Buck, Michael D., Buckton, Andrew, Budd, Timothy, Burrell, Alana, Busby, Louise, Bussi, Claudio, Butterworth, Simon, Byrne, Fiona, Campbell, Joanna, Canton, Johnathan, Cardoso, Ana, Carter, Nick, Carvalho, Luiz, Carzaniga, Raffaella, Chandler, Natalie, Chen, Qu, Clayton, Bobbi, Gigli, Clementina Cobolli, Collins, Zena, Cottrell, Sally, Cullup, Tom, Davies, Heledd, Davis, Patrick, Davison, Dara, Debaisieux, Solene, Diaz-Romero, Monica, Dibbs, Alison, Diring, Jessica, Driscoll, Paul C., D’Avola, Annalisa, Evangelopoulos, Dimitrios, Faraway, Rupert, Fearns, Antony, Ferron, Aaron, Dan Fitz, Fleming, James, Frederico, Bruno, Gait, Anthony, Gaul, Liam, Golding, Helen M., Gomez Dominguez, Belen, Gong, Hui, Grobler, Mariana, Guedan, Anabel, Gutierrez, Maximiliano G., Hackett, Fiona, Hall, Ross, Halldorsson, Steinar, Harris, Suzanne, Hashim, Sugera, Healy, Lyn, Herbst, Susanne, Hewitt, Graeme, Higgins, Theresa, Hirani, Rajnika, Hope, Joshua, Horton, Elizabeth, Hoskins, Beth, Howitt, Louise, Hoyle, Jacqueline, Htun, Mint R., Huerga Encabo, Hector, Hughes, Jane, Huseynova, Almaz, Hwang, Ming-Shih, Jenkins, Lucy, Kiely, Louise, King Spert Teixeira, Anastacio, Knuepfer, Ellen, Komarov, Nikita, Kotzampaltiris, Paul, Kousis, Konstantinos, Krylova, Tammy, Kucharska, Ania, Labrum, Robyn, Lambe, Catherine, Lappin, Michelle, Lee, Stacey-Ann, Liu, Hon Wing, Loughlin, Sam, Madoo, Akshay, Marczak, Julie A., Martensson, Mimmi, Martinez, Thomas, Marzook, Bishara, Matz, Joachim M., McCall, Samuel, McKay, Fiona, McNamara, Edel C., Minutti, Carlos M., Mistry, Gita, Molina-Arcas, Miriam, Montaner, Beatriz, Montgomery, Kylie, Moraiti, Anastasia, Moreira-Teixeira, Lucia, Mukherjee, Joyita, Naceur-Lombardelli, Cristina, Nelson, Aileen, Nofal, Stephanie, Nurse, Paul, Nutan, Savita, Oedekoven, Caroline, O’Garra, Anne, O’Leary, Jean D., O’Neill, Olga, Suarez, Paula Ordonez, Osborne, Neil, Pajak, Aleksandra, Patel, Yogen, Paun, Oana, Peces-Barba Castano, Laura, Perez Caballero, Ana, Perez-Lloret, Jimena, Perrault, Magali S., Perrin, Abigail, Poh, Roy, Poirier, Enzo Z., Polke, James M., Prieto-Godino, Lucia, Proust, Alize, Puvirajasinghe, Clinda, Queval, Christophe, Ramachandran, Vijaya, Ramaprasad, Abhinay, Reed, Laura, Richardson, Kayleigh, Ridewood, Sophie, Roberts, Fiona, Roberts, Rowenna, Rodgers, Angela, Clavijo, Pablo Romero, Rossi, Alice, Sahai, Erik, Sait, Aaron, Sala, Katarzyna, Sanderson, Theo, Santucci, Pierre, Sardar, Fatima, Sateriale, Adam, Saunders, Jill A., Sawyer, Chelsea, Schlott, Anja, Schweighoffer, Edina, Segura-Bayona, Sandra, Shah Punatar, Rajvee, Shaw, Joe, Silva Dos Santos, Mariana, Silvestre, Margaux, Singer, Matthew, Steel, Louisa, Sullivan, Adrienne E., Tan, Michele S. Y., Tautz-Davis, Zoe H., Taylor, Effie, Taylor, Gunes, Taylor, Harriet B., Taylor-Beadling, Alison, Teixeira Subtil, Fernanda, Terré Torras, Berta, Toolan-Kerr, Patrick, Torelli, Francesca, Toteva, Tea, Treeck, Moritz, Trojer, Hadija, Tsai, Ming-Han C., Ule, Jernej, Ulferts, Rachel, Vanloo, Sharon P., Veeriah, Selvaraju, Venkatesan, Subramanian, Vousden, Karen, Walder, Claire, Wang, Yiran, Wenman, Catharina, Williams, Luke, Williams, Matthew J., Wynne, Lauren, Xiang, Zheng, Yap, Melvyn, Zagalak, Julian A., Zecchin, Davide, and Zillwood, Rachel

Subjects
2019-20 coronavirus outbreak, Coronavirus disease 2019 (COVID-19), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Crick COVID-19 Consortium, Biomedical Engineering, Bioengineering, CORONAVIRUS, medicine.disease_cause, Applied Microbiology and Biotechnology, medicine, Medical Laboratory Science, Humans, Royaume uni, Coronavirus, Reino unido, Science & Technology, business.industry, Clinical Laboratory Techniques, Reverse Transcriptase Polymerase Chain Reaction, Academies and Institutes, Virology, United Kingdom, Europe, Biotechnology & Applied Microbiology, Molecular Medicine, business, Coronavirus Infections, Life Sciences & Biomedicine, Biotechnology, PNEUMONIA OUTBREAK
Published
2020

120. A Transcriptomic Profile of the Proximal Airway Epithelial-Immune Niche in Idiopathic Pulmonary Fibrosis

Author

Franz Puttur, Anne O'Garra, Richard J. Hewitt, Poonam Ghai, Christine M. Graham, Clare M. Lloyd, Philip L. Molyneaux, Adam J. Byrne, Patricia P. Ogger, Toby M. Maher, J. Perez-Lloret, and S.V. Kemp

Subjects
Transcriptome, Idiopathic pulmonary fibrosis, Immune system, business.industry, Immunology, Niche, Medicine, business, Airway, medicine.disease
Published
2020
Full Text
View/download PDF

121. Transcriptomic characterization of tuberculous sputum reveals a host Warburg effect and microbial cholesterol catabolism

Author

Neesha Rockwood, Anne O'Garra, Rachel P. J. Lai, Melissa L Burke, Douglas B. Young, Robert J. Wilkinson, Stuart Horswell, Teresa Cortes, Suzaan Marais, and Acely Garza-Garcia

Subjects
0303 health sciences, Tuberculosis, 030306 microbiology, Transmission (medicine), Biology, biology.organism_classification, medicine.disease, Warburg effect, 3. Good health, Microbiology, Mycobacterium tuberculosis, Transcriptome, 03 medical and health sciences, Regulon, medicine, Coinfection, Sputum, medicine.symptom, 030304 developmental biology
Abstract

The crucial transmission phase of tuberculosis (TB) relies on infectious sputum yet cannot easily be modeled. We applied one-step RNA-Sequencing to sputum from infectious TB patients to investigate the host and microbial environments underlying transmission of Mycobacterium tuberculosis (Mtb). In such TB sputa, compared to non-TB controls, transcriptional upregulation of inflammatory responses and a metabolic shift towards glycolysis was observed in the host. Amongst all bacterial sequences in the sputum, only less than 1.5% originated from Mtb and its abundance is associated with HIV-1 coinfection status. The transcriptome of sputum Mtb more closely resembled aerobic replication and was characterized by evidence of cholesterol utilization, zinc deprivation and reduced expression of the virulence-associated PhoP regulon. Our study provides a comprehensive analysis of the transcriptional landscape associated with infectious sputum and demonstrates the feasibility of applying advanced sequencing technology to readily accessible pathological specimens in the study of host-pathogen adaptation.

Published
2020
Full Text
View/download PDF

122. Preferences for water treatment provision in rural India: comparing communal, pay-per-use, and labour-for-water schemes

Author

Alfredo, Katherine Ann and O'Garra, Tanya

Abstract

Using a contingent valuation survey, this research identifies villagers’ willingness to pay towards the operation and maintenance of water treatment plants in 11 villages in Maharashtra with existing facilities. Preferences were elicited using three different payment mechanisms: a monthly fee, labour (time) contributions, and a pay-per-container mechanism. There was little support for the pay-per-container scheme (51% stated positive willingness to pay for this option), but the communal mechanisms were more popular (86.7% and 87.3%). We conclude that the long-term viability of water treatment in Maharashtra is weak, as few scenarios provide adequate revenue to properly operate and maintain the infrastructure.

Published
2020

123. Willingness to Reduce Travel Consumption to Support a Low-Carbon Transition Beyond COVID-19

Author

Roger Fouquet and Tanya O'Garra

Subjects
Consumption (economics), Overconsumption, Coronavirus disease 2019 (COVID-19), Income distribution, Turnover, Greenhouse gas, Survey data collection, Sample (statistics), Business, Agricultural economics
Abstract

This paper explores people’s willingness to reduce travel consumption in support of the transition to a low-carbon pathway beyond COVID-19 using new survey data from UK car drivers and air travellers. Over half (56%) of the car survey sample, and 45% of the air survey sample are willing to reduce the amount travelled by car and plane respectively beyond COVID-19, with mean stated reductions representing 24% and 20% of the pre-COVID-19 distance travelled per year by car and air. We estimate these travel reductions could lead to an average reduction of 486-551kgCO2 per car driver per year (or 20.2% - 22.9% of current emissions), and 225-354kgCO2 (9.7%-15.3% of current emissions) per air traveller per year. There is little difference in voluntary travel reductions across the income distribution, despite the top income quintile being responsible for 17% more car emissions and 87% more air travel emissions than the second-highest income quintile. Regressions show that pre-existing environmental values (proxied by membership of an environmental organisation) and the experience of having ‘more time to do creative things’ during the COVID-19 lockdown positively influence voluntary reductions. This paper concludes that policies to tackle emissions must address overconsumption associated with affluence, and must also seek ways to increase low-carbon leisure time.

Published
2020
Full Text
View/download PDF

124. Transcriptomic analysis reveals diverse gene expression changes in airway macrophages during experimental allergic airway disease

Author

Clare M. Lloyd, Anne O'Garra, and William J. Branchett

Subjects
0301 basic medicine, Chemokine, Macrophage, Population, Medicine (miscellaneous), General Biochemistry, Genetics and Molecular Biology, lung, Biological pathway, Transcriptome, 03 medical and health sciences, transcriptomics, 0302 clinical medicine, Gene expression, mouse models, education, house dust mite, education.field_of_study, Innate immune system, biology, Articles, asthma, allergy, Phenotype, 030104 developmental biology, airway, Immunology, biology.protein, Tumor necrosis factor alpha, Research Article, 030215 immunology
Abstract

Background: Airway macrophages (AMs) are the most abundant leukocytes in the healthy airway lumen and have a highly specialised but plastic phenotype that is governed by signals in the local microenvironment. AMs are thought to maintain immunological homeostasis in the steady state, but have also been implicated in the pathogenesis of allergic airway disease (AAD). In this study, we aimed to better understand these potentially contrasting AM functions using transcriptomic analysis. Methods: Bulk RNA sequencing was performed on AMs (CD11c+ Siglec F+ CD64+ CD45+ SSChi) flow cytometry sorted from C57BL/6 mice during experimental AAD driven by repeated house dust mite inhalation (AMs HDM), compared to control AMs from non-allergic mice. Differentially expressed genes were further analysed by hierarchical clustering and biological pathway analysis. Results: AMs HDM showed increased expression of genes associated with antigen presentation, inflammatory cell recruitment and tissue repair, including several chemokine and matrix metalloproteinase genes. This was accompanied by increased expression of mitochondrial electron transport chain subunit genes and the retinoic acid biosynthetic enzyme gene Raldh2. Conversely, AMs HDM displayed decreased expression of a number of cell cycle genes, genes related to cytoskeletal functions and a subset of genes implicated in antimicrobial innate immunity, such as Tlr5, Il18 and Tnf. Differential gene expression in AMs HDM was consistent with upstream effects of the cytokines IL-4 and IFN-γ, both of which were present at increased concentrations in lung tissue after HDM treatment. Conclusions: These data highlight diverse gene expression changes in the total AM population in a clinically relevant mouse model of AAD, collectively suggestive of contributions to inflammation and tissue repair/remodelling, but with decreases in certain steady state cellular and immunological functions.

Published
2020

125. Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis

Author

Iker Valle Aramburu, Margarida Saraiva, Anne O'Garra, Marianna Ioannou, Lúcia Moreira-Teixeira, Evangelos Stavropoulos, Qian Wang, Alejandro Suárez-Bonnet, Philippa J. Stimpson, Venizelos Papayannopoulos, Cristina Vilaplana, Kaori L. Fonseca, Probir Chakravarty, Eleanor Herbert, Paula Rodríguez-Martínez, Simon L. Priestnall, Sabelo Hadebe, Sergo Vashakidze, Jeremy Sousa, and Instituto de Investigação e Inovação em Saúde

Subjects
0301 basic medicine, Neutrophils, medicine.medical_treatment, General Physics and Astronomy, Neutrophils / immunology, Receptor, Interferon alpha-beta, Disease, Interferon Type I / metabolism, Interferon-gamma / genetics, Receptor, Interferon alpha-beta / genetics, Extracellular Traps, Pathogenesis, Mice, 0302 clinical medicine, Tuberculosis, Pulmonary / microbiology, Databases, Genetic, RNA-Seq, lcsh:Science, Lung, Mice, Knockout, Multidisciplinary, biology, Tuberculosis, Pulmonary / genetics, Receptor, Interferon alpha-beta / metabolism, Pneumonia / immunology, Pneumonia / genetics, Mycobacterium tuberculosis / pathogenicity, 3. Good health, Interferon-gamma / metabolism, Cytokine, Interferon Type I, Disease Progression, Cytokines, Infectious diseases, medicine.symptom, Infection, Interferon Type I / genetics, Pneumonia / metabolism, Tuberculosis, Pulmonary / blood, Tuberculosis, Science, Immunology, Inflammation, Article, General Biochemistry, Genetics and Molecular Biology, Mycobacterium tuberculosis, Interferon-gamma, 03 medical and health sciences, Granulocyte-Macrophage Colony-Stimulating Factor / metabolism, Lung / pathology, medicine, Lung / immunology, Animals, Humans, Tuberculosis, Pulmonary / immunology, Tuberculosis, Pulmonary, Innate immune system, business.industry, Gene Expression Profiling, Granulocyte-Macrophage Colony-Stimulating Factor, Pneumonia, General Chemistry, Neutrophil extracellular traps, Mycobacterium tuberculosis / immunology, biology.organism_classification, medicine.disease, Pneumonia / pathology, Mice, Inbred C57BL, 030104 developmental biology, Extracellular Traps / immunology, lcsh:Q, Lung / microbiology, business, Lung / metabolism, 030215 immunology, Granulocyte-Macrophage Colony-Stimulating Factor / genetics
Abstract

Tuberculosis (TB) is a leading cause of mortality due to infectious disease, but the factors determining disease progression are unclear. Transcriptional signatures associated with type I IFN signalling and neutrophilic inflammation were shown to correlate with disease severity in mouse models of TB. Here we show that similar transcriptional signatures correlate with increased bacterial loads and exacerbate pathology during Mycobacterium tuberculosis infection upon GM-CSF blockade. Loss of GM-CSF signalling or genetic susceptibility to TB (C3HeB/FeJ mice) result in type I IFN-induced neutrophil extracellular trap (NET) formation that promotes bacterial growth and promotes disease severity. Consistently, NETs are present in necrotic lung lesions of TB patients responding poorly to antibiotic therapy, supporting the role of NETs in a late stage of TB pathogenesis. Our findings reveal an important cytokine-based innate immune effector network with a central role in determining the outcome of M. tuberculosis infection., GM-CSF is involved in control over M. tuberculosis infection. Here the authors show that GM-CSF reduces type 1 interferon driven neutrophil recruitment, NETosis and bacterial growth in the lungs of infected mice, and provide evidence that this NETosis occurs in infected humans who are not responsive to antibiotic therapy.

Published
2020

126. The Behavioural, Welfare and Environmental Effects of Air Travel Reductions During and Beyond COVID-19

Author

Roger Fouquet and Tanya O'Garra

Subjects
2019-20 coronavirus outbreak, Carbon tax, Inequality, Coronavirus disease 2019 (COVID-19), media_common.quotation_subject, Development economics, Pandemic, Economics, Current (fluid), Welfare, media_common, Air travel
Abstract

Given the disruption in air travel due to the COVID-19 pandemic, we are faced with a unique opportunity to examine to what extent current reduced levels of avia

Published
2020
Full Text
View/download PDF

127. Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.

Author

Sonja Tattermusch, Jason A Skinner, Damien Chaussabel, Jacques Banchereau, Matthew P Berry, Finlay W McNab, Anne O'Garra, Graham P Taylor, and Charles R M Bangham

Subjects
Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that persists lifelong in the host. In ∼4% of infected people, HTLV-1 causes a chronic disabling neuroinflammatory disease known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The pathogenesis of HAM/TSP is unknown and treatment remains ineffective. We used gene expression microarrays followed by flow cytometric and functional assays to investigate global changes in blood transcriptional profiles of HTLV-1-infected and seronegative individuals. We found that perturbations of the p53 signaling pathway were a hallmark of HTLV-1 infection. In contrast, a subset of interferon (IFN)-stimulated genes was over-expressed in patients with HAM/TSP but not in asymptomatic HTLV-1 carriers or patients with the clinically similar disease multiple sclerosis. The IFN-inducible signature was present in all circulating leukocytes and its intensity correlated with the clinical severity of HAM/TSP. Leukocytes from patients with HAM/TSP were primed to respond strongly to stimulation with exogenous IFN. However, while type I IFN suppressed expression of the HTLV-1 structural protein Gag it failed to suppress the highly immunogenic viral transcriptional transactivator Tax. We conclude that over-expression of a subset of IFN-stimulated genes in chronic HTLV-1 infection does not constitute an efficient host response but instead contributes to the development of HAM/TSP.

Published
2012
Full Text
View/download PDF

128. IL-10 regulates viral lung immunopathology during acute respiratory syncytial virus infection in mice.

Author

Jens Loebbermann, Corinna Schnoeller, Hannah Thornton, Lydia Durant, Nathan P Sweeney, Martijn Schuijs, Anne O'Garra, Cecilia Johansson, and Peter J Openshaw

Subjects
Medicine, Science
Abstract

Interleukin (IL-) 10 is a pleiotropic cytokine with broad immunosuppressive functions, particularly at mucosal sites such as the intestine and lung. Here we demonstrate that infection of BALB/c mice with respiratory syncytial virus (RSV) induced IL-10 production by CD4(+) and CD8(+) T cells in the airways at later time points (e.g. day 8); a proportion of these cells also co-produced IFN-γ. Furthermore, RSV infection of IL-10(-/-) mice resulted in more severe disease with enhanced weight loss, delayed recovery and greater cell infiltration of the respiratory tract without affecting viral load. In addition, IL-10(-/-) mice had a pronounced airway neutrophilia and heightened levels of pro-inflammatory cytokines and chemokines in the bronchoalveolar lavage fluid. Notably, the proportion of lung T cells producing IFN-γ was enhanced, suggesting that IL-10 may act in an autocrine manner to dampen effector T cell responses. Similar findings were made in mice treated with anti-IL-10R antibody and infected with RSV. Therefore, IL-10 inhibits disease and inflammation in mice infected with RSV, especially during recovery from infection.

Published
2012
Full Text
View/download PDF

129. Detectable changes in the blood transcriptome are present after two weeks of antituberculosis therapy.

Author

Chloe I Bloom, Christine M Graham, Matthew P R Berry, Katalin A Wilkinson, Tolu Oni, Fotini Rozakeas, Zhaohui Xu, Jose Rossello-Urgell, Damien Chaussabel, Jacques Banchereau, Virginia Pascual, Marc Lipman, Robert J Wilkinson, and Anne O'Garra

Subjects
Medicine, Science
Abstract

Globally there are approximately 9 million new active tuberculosis cases and 1.4 million deaths annually. Effective antituberculosis treatment monitoring is difficult as there are no existing biomarkers of poor adherence or inadequate treatment earlier than 2 months after treatment initiation. Inadequate treatment leads to worsening disease, disease transmission and drug resistance.To determine if blood transcriptional signatures change in response to antituberculosis treatment and could act as early biomarkers of a successful response.Blood transcriptional profiles of untreated active tuberculosis patients in South Africa were analysed before, during (2 weeks and 2 months), at the end of (6 months) and after (12 months) antituberculosis treatment, and compared to individuals with latent tuberculosis. An active-tuberculosis transcriptional signature and a specific treatment-response transcriptional signature were derived. The specific treatment response transcriptional signature was tested in two independent cohorts. Two quantitative scoring algorithms were applied to measure the changes in the transcriptional response. The most significantly represented pathways were determined using Ingenuity Pathway Analysis.An active tuberculosis 664-transcript signature and a treatment specific 320-transcript signature significantly diminished after 2 weeks of treatment in all cohorts, and continued to diminish until 6 months. The transcriptional response to treatment could be individually measured in each patient.Significant changes in the transcriptional signatures measured by blood tests were readily detectable just 2 weeks after treatment initiation. These findings suggest that blood transcriptional signatures could be used as early surrogate biomarkers of successful treatment response.

Published
2012
Full Text
View/download PDF

132. The effect of anchors and social information on behaviour

Author

O'Garra, Tanya, Sisco, Matthew R., O'Garra, Tanya, and Sisco, Matthew R.

Abstract

We use a ‘multi-player dictator game’ (MDG), with ‘social information’ about the monetary transfer made by a previous dictator to a recipient, to examine whether average contributions as well as the behavioural strategy adopted are affected by the first amount presented (the ‘anchor’) using a sequential strategy elicitation method. We find that average contributions are positively affected by the anchor. The anchor is also found to influence the behavioural strategy that individuals adopt, such that low anchors significantly increase the likelihood that players will adopt unconditional self-interested strategies, whereas high anchors increase the likelihood of adopting giving strategies. The distribution of strategies – and hence, the distribution of behavioural ‘types’ - is therefore affected by the initial conditions of play, lending support to the notion that behavioural strategies are context dependent.

Published
2020

134. A modular transcriptional signature identifies phenotypic heterogeneity of human tuberculosis infection

Author

Christine M. Graham, Gerrit Woltmann, Anne O'Garra, Pranabashis Haldar, Akul Singhania, Trang Tran, Matthew Berry, Marc Rodrigue, Patrick Lecine, Philippe Leissner, Robert J. Wilkinson, Raman Verma, Matthew Richardson, Karine Kaiser, Jo Lee, and Wellcome Trust

Subjects
Male, 0301 basic medicine, TBX21, BACTERIAL, BLOOD, Transcription, Genetic, Microarray, General Physics and Astronomy, SUSCEPTIBILITY, EXPRESSION PROFILES, Cohort Studies, Transcriptome, 0302 clinical medicine, IMMUNE-RESPONSE, Longitudinal Studies, 030212 general & internal medicine, lcsh:Science, Oligonucleotide Array Sequence Analysis, 0303 health sciences, Multidisciplinary, GAMMA RELEASE ASSAYS, Middle Aged, 3. Good health, Multidisciplinary Sciences, Improved performance, Phenotype, Area Under Curve, Science & Technology - Other Topics, Female, MYCOBACTERIAL INFECTION, Immunosuppressive Agents, Adult, Risk, Tuberculosis, Science, Computational biology, Biology, General Biochemistry, Genetics and Molecular Biology, Interferon-gamma, 03 medical and health sciences, medicine, Humans, Diagnostic biomarker, Tuberculosis, Pulmonary, Gene, 030304 developmental biology, Aged, Gene Library, Science & Technology, Sequence Analysis, RNA, Genetic heterogeneity, Gene Expression Profiling, Mycobacterium tuberculosis, General Chemistry, ACTIVE TUBERCULOSIS, medicine.disease, GENE, Gene selection, 030104 developmental biology, ROC Curve, Immunology, lcsh:Q, T-Box Domain Proteins, RESISTANCE, Biomarkers, 030215 immunology
Abstract

Whole blood transcriptional signatures distinguishing active tuberculosis patients from asymptomatic latently infected individuals exist. Consensus has not been achieved regarding the optimal reduced gene sets as diagnostic biomarkers that also achieve discrimination from other diseases. Here we show a blood transcriptional signature of active tuberculosis using RNA-Seq, confirming microarray results, that discriminates active tuberculosis from latently infected and healthy individuals, validating this signature in an independent cohort. Using an advanced modular approach, we utilise the information from the entire transcriptome, which includes overabundance of type I interferon-inducible genes and underabundance of IFNG and TBX21, to develop a signature that discriminates active tuberculosis patients from latently infected individuals or those with acute viral and bacterial infections. We suggest that methods targeting gene selection across multiple discriminant modules can improve the development of diagnostic biomarkers with improved performance. Finally, utilising the modular approach, we demonstrate dynamic heterogeneity in a longitudinal study of recent tuberculosis contacts.

Published
2018

135. Progression of whole blood transcriptional signatures from interferon-induced to neutrophil-associated patterns in patients with severe influenza

Author

Dunning, J, Blankley, S, Hoang, LT, Cox, M, Graham, CM, James, PL, Bloom, CI, Chaussabel, D, Banchereau, J, Brett, SJ, Moffatt, MF, Habibi, MS, Johnston, SL, Hansel, TT, Levin, M, Thwaites, RS, Warner, JO, Cookson, WO, Gazzard, BG, Hay, A, McCauley, J, Aylin, P, Ashby, D, Barclay, WS, Elderfield, RA, Nadel, S, Herberg, JA, Drumright, LN, Garcia-Alvarez, L, Holmes, AH, Kon, OM, Aston, SJ, Gordon, SB, Hussell, T, Thompson, C, Zambon, MC, Baillie, KJ, Hume, DA, Simmonds, P, Hayward, A, Smyth, RL, McNamara, PS, Semple, MG, Nguyen-Van-Tam, JS, Ho, LP, McMichael, AJ, Kellam, P, Adamson, WE, Carman, WF, Griffiths, MJ, O'Garra, A, Openshaw, PJM, Wellcome Trust, National Institute for Health Research, Medical Research Council (MRC), and Asthma UK

Subjects
0301 basic medicine, Male, Neutrophils, Disease, DISEASE, Procalcitonin, Transcriptome, Pathogenesis, 0302 clinical medicine, MARKERS, Interferon, Immunology and Allergy, Medicine, MOSAIC Investigators, Young adult, UNITED-KINGDOM, Middle Aged, 3. Good health, 1107 Immunology, 030220 oncology & carcinogenesis, Disease Progression, Female, Life Sciences & Biomedicine, medicine.drug, Adult, Adolescent, Immunology, CIRCULATION, BIOLOGY, VIRUS-INFECTION, Lung injury, Antiviral Agents, Article, 03 medical and health sciences, Young Adult, Influenza, Human, Humans, RNA, Messenger, PROCALCITONIN, METAANALYSIS, Aged, Science & Technology, business.industry, Human genetics, 030104 developmental biology, Interferons, business, LUNG INJURY, Biomarkers
Abstract

© 2018 The Author(s). Transcriptional profiles and host-response biomarkers are used increasingly to investigate the severity, subtype and pathogenesis of disease. We now describe whole-blood mRNA signatures and concentrations of local and systemic immunological mediators in 131 adults hospitalized with influenza, from whom extensive clinical and investigational data were obtained by MOSAIC investigators. Signatures reflective of interferon-related antiviral pathways were common up to day 4 of symptoms in patients who did not require mechanical ventilator support; in those who needed mechanical ventilation, an inflammatory, activated-neutrophil and cell-stress or death ('bacterial') pattern was seen, even early in disease. Identifiable bacterial co-infection was not necessary for this 'bacterial' signature but was able to enhance its development while attenuating the early 'viral' signature. Our findings emphasize the importance of timing and severity in the interpretation of host responses to acute viral infection and identify specific patterns of immune-system activation that might enable the development of novel diagnostic and therapeutic tools for severe influenza.

Published
2018

136. Type I interferons in tuberculosis: Foe and occasionally friend

Author

Alan Sher, Lúcia Moreira-Teixeira, Katrin D. Mayer-Barber, and Anne O'Garra

Subjects
0301 basic medicine, Tuberculosis, Immunology, Reviews, Review, Models, Biological, Mycobacterium tuberculosis, 03 medical and health sciences, 0302 clinical medicine, Immune system, Immunity, medicine, Animals, Humans, Immunology and Allergy, Clinical significance, Gene, biology, business.industry, 11 Medical And Health Sciences, Active tuberculosis, medicine.disease, biology.organism_classification, 3. Good health, Disease Models, Animal, 030104 developmental biology, Interferon Type I, business, Interferon type I, 030215 immunology, medicine.drug
Abstract

Type I interferons have been implicated in the pathogenesis of tuberculosis. Herein, Moreira-Teixeira et al. discuss mechanistic and contextual factors that determine the role of type I interferons during Mycobacterium tuberculosis infection, from human disease to experimental models of tuberculosis., Tuberculosis remains one of the leading causes of mortality worldwide, and, despite its clinical significance, there are still significant gaps in our understanding of pathogenic and protective mechanisms triggered by Mycobacterium tuberculosis infection. Type I interferons (IFN) regulate a broad family of genes that either stimulate or inhibit immune function, having both host-protective and detrimental effects, and exhibit well-characterized antiviral activity. Transcriptional studies have uncovered a potential deleterious role for type I IFN in active tuberculosis. Since then, additional studies in human tuberculosis and experimental mouse models of M. tuberculosis infection support the concept that type I IFN promotes both bacterial expansion and disease pathogenesis. More recently, studies in a different setting have suggested a putative protective role for type I IFN. In this study, we discuss the mechanistic and contextual factors that determine the detrimental versus beneficial outcomes of type I IFN induction during M. tuberculosis infection, from human disease to experimental mouse models of tuberculosis.

Published
2018
Full Text
View/download PDF

137. B Cells Producing Type I IFN Modulate Macrophage Polarization in Tuberculosis

Author

Andre G. Loxton, Pablo Schierloh, Ingrid Mercier, Jan Rehwinkel, Brigitte Gicquel, Véronique Anton-Leberre, Talal Al-Saati, María del Carmen Sasiain, Anne O'Garra, Pierre Boudinot, Ludovic Tailleux, Olivier Neyrolles, Roland Lang, André Colom, Stefan H. E. Kaufmann, Simon Fillatreau, Alan Bénard, Denis Hudrisier, Luc Jouneau, Imme Sakwa, Institut de pharmacologie et de biologie structurale (IPBS), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Immunometabolism and Macrophages in Tuberculosis/Human Immunodeficiency Virus-1 Co-infection (LIA IM-TB/HIV), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Academia Nacional de Medicina, Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), Deutsches Rheuma-ForschungsZentrum, Academia Nacional de Medicina, Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés (LISBP), Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Pathogénomique mycobactérienne intégrée, Institut Pasteur [Paris] (IP), Unité de recherche Virologie et Immunologie Moléculaires (VIM (UR 0892)), Institut National de la Recherche Agronomique (INRA), Centre Régional d'Exploration Fonctionnelle et Ressources Expérimentales (CREFRE), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), University of Oxford, Stellenbosch University, Max Planck Institute for Infection Biology (MPIIB), Max-Planck-Gesellschaft, Nationale Institute for Medical Research, Imperial College London, Deutsches RheumaForschungszentrum, Leibniz Institute - German Rheumatism Research Centre (DRFZ), Supported by Centre National de la Recherche Scientifique, University of Toulouse–Université Paul Sabatier, Institut Pasteur, Agence Nationale de la Recherche grants B-TB ANR-12-BSV3-0002 and ANR-11-EQUIPEX-0003 (O.N.), the European Union grants NEWTBVAC 241745 and TBVAC2020 643381 (O.N. and S.H.E.K.), grant ERA-INFECT ABIR (S.F. and S.H.E.K), the Bettencourt-Schueller Foundation, the Fondation pour la Recherche Médicale grant DEQ20160334902 (O.N.), and Deutsche Forschungsgemeinschaft grants SFB 796 and TP B6 (R.L.) and SFB TRR10 (S.F.). A.O’G. is funded by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001126), the UK Medical Research Council (FC001126), and the Wellcome Trust (FC001126), by the UK Medical Research Council (MR/U117565642/1), and by the European Research Council (294682-TB-PATH). A.B. held a fellowship from the Fondation pour la Recherche Médicale., ANR-12-BSV3-0002,B-TB,Rôle des lymphocytes B dans l'immunité et l'inflammation tuberculeuse(2012), ANR-11-EQPX-0011,CRITEX,Parc national d'équipements innovants pour l'étude spatiale et temporelle de la Zone Critique des Bassins Versants(2011), European Project: 241745,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,NEWTBVAC(2010), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Immunometabolism and Macrophages in Tuberculosis/Human Immunodeficiency Virus-1 Co-infection (IM-TB/HIV), Centre National de la Recherche Scientifique (CNRS)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Recherche Agronomique (INRA), Institut Pasteur [Paris], Unité de recherche Virologie et Immunologie Moléculaires (VIM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], University of Oxford [Oxford], Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées

Subjects
0301 basic medicine, Pulmonary and Respiratory Medicine, CIENCIAS MÉDICAS Y DE LA SALUD, Tuberculosis, [SDV]Life Sciences [q-bio], Inmunología, Macrophage polarization, TUBERCULOSIS, IFN, Critical Care and Intensive Care Medicine, Mice, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MACROPHAGES, Lung, B-Lymphocytes, business.industry, Editorials, food and beverages, Mycobacterium tuberculosis, B LYMPHOCYTES, medicine.disease, Virology, macrophages, 3. Good health, Mice, Inbred C57BL, B-1 cell, Disease Models, Animal, Medicina Básica, 030104 developmental biology, tuberculosis, Interferon Type I, Immunology, business, Spleen, Function (biology), Signal Transduction, B lymphocytes, 030215 immunology
Abstract

In addition to their well-known function as antibody-producing cells, B lymphocytes can markedly influence the course of infectious or noninfectious diseases via antibody-independent mechanisms. In tuberculosis (TB), B cells accumulate in lungs, yet their functional contribution to the host response remains poorly understoo Fil: Bénard, Alan. Centre National de la Recherche Scientifique; Francia Fil: Sakwa, Imme. Leibniz - Institute Of Freshwater Ecology And Inland Fisheries; Alemania Fil: Schierloh, Luis Pablo. Instituto National de Recherches Agronomiques. Centre de Recherches de Toulouse; Francia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Colom, André. Centre National de la Recherche Scientifique; Francia Fil: Mercier, Ingrid. Instituto National de Recherches Agronomiques. Centre de Recherches de Toulouse; Francia Fil: Tailleux, Ludovic. Instituto Pasteur; Francia Fil: Jouneau, Luc. Institut National de la Recherche Agronomique; Francia Fil: Boudinot, Pierre. Institut National de la Recherche Agronomique; Francia Fil: Al Saati, Talal. Université Paul Sabatier; Francia Fil: Lang, Roland. Universitat Erlangen-Nuremberg; Alemania Fil: Rehwinkel, Jan. University of Oxford; Reino Unido Fil: Loxton, Andre G.. Stellenbosch University; Sudáfrica Fil: Kaufmann, Stefan H. E.. Max Planck Institut für Infektionsbiologie; Alemania Fil: Anton Leberre, Veronique. Institut National de la Recherche Agronomique; Francia Fil: O'Garra, Anne. National Institute for Medical Research; Reino Unido Fil: Sasiain, María del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Gicquel, Brigitte. Institut National de la Recherche Agronomique; Francia Fil: Fillatreau, Simon. Centre National de la Recherche Scientifique; Francia Fil: Neyrolles, Olivier. Centre National de la Recherche Scientifique; Francia Fil: Hudrisier, Denis. Centre National de la Recherche Scientifique; Francia

Published
2018
Full Text
View/download PDF

140. Clinical outcomes of COVID-19 in long-term care facilities for people with epilepsy

Author

Balestrini, Simona, primary, Koepp, Matthias J., additional, Gandhi, Sonia, additional, Rickman, Hannah M., additional, Shin, Gee Yen, additional, Houlihan, Catherine F., additional, Anders-Cannon, Jonny, additional, Silvennoinen, Katri, additional, Xiao, Fenglai, additional, Zagaglia, Sara, additional, Hudgell, Kirsty, additional, Ziomek, Mariusz, additional, Haimes, Paul, additional, Sampson, Adam, additional, Parker, Annie, additional, Helen Cross, J., additional, Pardington, Rosemarie, additional, Nastouli, Eleni, additional, Swanton, Charles, additional, Sander, Josemir W., additional, Sisodiya, Sanjay M., additional, Aitken, Jim, additional, Allen, Zoe, additional, Ambler, Rachel, additional, Ambrose, Karen, additional, Ashton, Emma, additional, Avola, Alida, additional, Balakrishnan, Samutheswari, additional, Barns-Jenkins, Caitlin, additional, Barr, Genevieve, additional, Barrell, Sam, additional, Basu, Souradeep, additional, Beale, Rupert, additional, Beesley, Clare, additional, Bhardwaj, Nisha, additional, Bibi, Shahnaz, additional, Bineva-Todd, Ganka, additional, Biswas, Dhruva, additional, Blackman, Michael J., additional, Bonnet, Dominique, additional, Bowker, Faye, additional, Broncel, Malgorzata, additional, Brooks, Claire, additional, Buck, Michael D., additional, Buckton, Andrew, additional, Budd, Timothy, additional, Burrell, Alana, additional, Busby, Louise, additional, Bussi, Claudio, additional, Butterworth, Simon, additional, Byott, Matthew, additional, Byrne, Fiona, additional, Byrne, Richard, additional, Caidan, Simon, additional, Campbell, Joanna, additional, Canton, Johnathan, additional, Cardoso, Ana, additional, Carter, Nick, additional, Carvalho, Luiz, additional, Carzaniga, Raffaella, additional, Chandler, Natalie, additional, Chen, Qu, additional, Cherepanov, Peter, additional, Churchward, Laura, additional, Clark, Graham, additional, Clayton, Bobbi, additional, Cobolli Gigli, Clementina, additional, Collins, Zena, additional, Cottrell, Sally, additional, Crawford, Margaret, additional, Cubitt, Laura, additional, Cullup, Tom, additional, Davies, Heledd, additional, Davis, Patrick, additional, Davison, Dara, additional, Dearing, Vicky, additional, Debaisieux, Solene, additional, Diaz-Romero, Monica, additional, Dibbs, Alison, additional, Diring, Jessica, additional, Driscoll, Paul C., additional, D'Avola, Annalisa, additional, Earl, Christopher, additional, Edwards, Amelia, additional, Ekin, Chris, additional, Evangelopoulos, Dimitrios, additional, Faraway, Rupert, additional, Fearns, Antony, additional, Ferron, Aaron, additional, Fidanis, Efthymios, additional, Fitz, Dan, additional, Fleming, James, additional, Frampton, Daniel, additional, Frederico, Bruno, additional, Gaiba, Alessandra, additional, Gait, Anthony, additional, Gamblin, Steve, additional, Gärtner, Kathleen, additional, Gaul, Liam, additional, Golding, Helen M., additional, Goldman, Jacki, additional, Goldstone, Robert, additional, Gomez Dominguez, Belen, additional, Gong, Hui, additional, Grant, Paul R., additional, Greco, Maria, additional, Grobler, Mariana, additional, Guedan, Anabel, additional, Gutierrez, Maximiliano G., additional, Hackett, Fiona, additional, Hall, Ross, additional, Halldorsson, Steinar, additional, Harris, Suzanne, additional, Hashim, Sugera, additional, Hatipoglu, Emine, additional, Healy, Lyn, additional, Heaney, Judith, additional, Herbst, Susanne, additional, Hewitt, Graeme, additional, Higgins, Theresa, additional, Hindmarsh, Steve, additional, Hirani, Rajnika, additional, Hope, Joshua, additional, Horton, Elizabeth, additional, Hoskins, Beth, additional, Howell, Michael, additional, Howitt, Louise, additional, Hoyle, Jacqueline, additional, Htun, Mint R., additional, Hubank, Michael, additional, Huerga Encabo, Hector, additional, Hughes, Deborah, additional, Hughes, Jane, additional, Huseynova, Almaz, additional, Hwang, Ming-Shih, additional, Instrell, Rachael, additional, Jackson, Deborah, additional, Jamal-Hanjani, Mariam, additional, Jenkins, Lucy, additional, Jiang, Ming, additional, Johnson, Mark, additional, Jones, Leigh, additional, Kanu, Nnennaya, additional, Kassiotis, George, additional, Kelly, Gavin, additional, Kiely, Louise, additional, Teixeira, Anastacio King Spert, additional, Kirk, Stuart, additional, Kjaer, Svend, additional, Knuepfer, Ellen, additional, Komarov, Nikita, additional, Kotzampaltiris, Paul, additional, Kousis, Konstantinos, additional, Krylova, Tammy, additional, Kucharska, Ania, additional, Labrum, Robyn, additional, Lambe, Catherine, additional, Lappin, Michelle, additional, Lee, Stacey-Ann, additional, Levett, Andrew, additional, Levett, Lisa, additional, Levi, Marcel, additional, Liu, Hon Wing, additional, Loughlin, Sam, additional, Lu, Wei-Ting, additional, MacRae, James I., additional, Madoo, Akshay, additional, Marczak, Julie A., additional, Martensson, Mimmi, additional, Martinez, Thomas, additional, Marzook, Bishara, additional, Matthews, John, additional, Matz, Joachim M., additional, McCall, Samuel, additional, McCoy, Laura E., additional, McKay, Fiona, additional, McNamara, Edel C., additional, Minutti, Carlos M., additional, Mistry, Gita, additional, Molina-Arcas, Miriam, additional, Montaner, Beatriz, additional, Montgomery, Kylie, additional, Moore, Catherine, additional, Moore, David, additional, Moraiti, Anastasia, additional, Moreira-Teixeira, Lucia, additional, Mukherjee, Joyita, additional, Naceur-Lombardelli, Cristina, additional, Nelson, Aileen, additional, Nicod, Jerome, additional, Nightingale, Luke, additional, Nofal, Stephanie, additional, Nurse, Paul, additional, Nutan, Savita, additional, Oedekoven, Caroline, additional, O'Garra, Anne, additional, O'Leary, Jean D., additional, Olsen, Jessica, additional, O'Neill, Olga, additional, O'Reilly, Nicola, additional, Suarez, Paula Ordonez, additional, Osborne, Neil, additional, Pabari, Amar, additional, Pajak, Aleksandra, additional, Papayannopoulos, Venizelos, additional, Paraskevopoulou, Stavroula M, additional, Patel, Namita, additional, Patel, Yogen, additional, Paun, Oana, additional, Peat, Nigel, additional, Peces-Barba Castano, Laura, additional, Caballero, Ana Perez, additional, Perez-Lloret, Jimena, additional, Perrault, Magali S., additional, Perrin, Abigail, additional, Poh, Roy, additional, Poirier, Enzo Z., additional, Polke, James M., additional, Pollitt, Marc, additional, Prieto-Godino, Lucia, additional, Proust, Alize, additional, Puvirajasinghe, Clinda, additional, Queval, Christophe, additional, Ramachandran, Vijaya, additional, Ramaprasad, Abhinay, additional, Ratcliffe, Peter, additional, Reed, Laura, additional, Reis e Sousa, Caetano, additional, Richardson, Kayleigh, additional, Ridewood, Sophie, additional, Roberts, Fiona, additional, Roberts, Rowenna, additional, Rodgers, Angela, additional, Romero Clavijo, Pablo, additional, Rosa, Annachiara, additional, Rossi, Alice, additional, Roustan, Chloe, additional, Rowan, Andrew, additional, Sahai, Erik, additional, Sait, Aaron, additional, Sala, Katarzyna, additional, Sanchez, Emilie, additional, Sanderson, Theo, additional, Santucci, Pierre, additional, Sardar, Fatima, additional, Sateriale, Adam, additional, Saunders, Jill A., additional, Sawyer, Chelsea, additional, Schlott, Anja, additional, Schweighoffer, Edina, additional, Segura-Bayona, Sandra, additional, Shah Punatar, Rajvee, additional, Shahmanesh, Maryam, additional, Shaw, Joe, additional, Silva Dos Santos, Mariana, additional, Silvestre, Margaux, additional, Singer, Matthew, additional, Snell, Daniel M., additional, Song, Ok-Ryul, additional, Spyer, Moira J., additional, Steel, Louisa, additional, Strange, Amy, additional, Sullivan, Adrienne E., additional, Tan, Michele S.Y., additional, Tautz-Davis, Zoe H., additional, Taylor, Effie, additional, Taylor, Gunes, additional, Taylor, Harriet B., additional, Taylor-Beadling, Alison, additional, Teixeira Subtil, Fernanda, additional, Terré Torras, Berta, additional, Toolan-Kerr, Patrick, additional, Torelli, Francesca, additional, Toteva, Tea, additional, Treeck, Moritz, additional, Trojer, Hadija, additional, Tsai, Ming-Han C., additional, Turner, James M.A., additional, Turner, Melanie, additional, Ule, Jernej, additional, Ulferts, Rachel, additional, Vanloo, Sharon P., additional, Veeriah, Selvaraju, additional, Venkatesan, Subramanian, additional, Vousden, Karen, additional, Wack, Andreas, additional, Walder, Claire, additional, Walker, Philip A., additional, Wang, Yiran, additional, Ward, Sophia, additional, Wenman, Catharina, additional, Williams, Luke, additional, Williams, Matthew J., additional, Keong Wong, Wai, additional, Wright, Joshua, additional, Wu, Mary, additional, Wynne, Lauren, additional, Xiang, Zheng, additional, Yap, Melvyn, additional, Zagalak, Julian A., additional, Zecchin, Davide, additional, Zillwood, Rachel, additional, Carthiyaniamma, Santhakumari, additional, DeTisi, Jane, additional, Dick, Julie, additional, Hill, Andrea, additional, Kipper, Karin, additional, Kullar, Birinder, additional, Norris, Sarah, additional, Rugg-Gunn, Fergus, additional, Salvatierra, Rebecca, additional, Shaya, Gabriel, additional, Sloan, Astrid, additional, Singh, Priyanka, additional, Varley, James, additional, and Whatley, Ben, additional

Published
2021
Full Text
View/download PDF

143. Blood Transcriptional Phenotypes of Progressive Latent M. tuberculosis Infection Inform Novel Signatures That Improve Prediction of Tuberculosis Risk

Author

Richardson, Matthew, primary, Verma, Raman, additional, Singhania, Akul, additional, Tabone, Olivier, additional, Das, Mrinal, additional, Rodrigue, Marc, additional, Leissner, Philippe, additional, Woltmann, Gerrit, additional, Cooper, Andrea, additional, O’Garra, Anne, additional, and Haldar, Pranabashis, additional

Published
2021
Full Text
View/download PDF

144. Regulatory T cells and mechanisms of immune system control

Author

O'Garra, Anne and Vieira, Paulo

Abstract

The immune system evolved to protect the host against the attack of foreign, potentially pathogenic, microorganisms. It does so by recognizing antigens expressed by those microorganisms and mounting an immune response against all cells expressing them, with the ultimate aim of their elimination. Various mechanisms have been reported to control and regulate the immune system to prevent or minimize reactivity to self-antigens or an overexuberant response to a pathogen, both of which can result in damage to the host. Deletion of autoreactive cells during T- and B-cell development allows the immune system to be tolerant of most self-antigens. Peripheral tolerance to self was suggested several years ago to result from the induction of anergy in peripheral self-reactive lymphocytes. More recently, however, it has become clear that avoidance of damage to the host is also achieved by active suppression mediated by regulatory T (T[sub.reg]) cell populations. We discuss here the varied mechanisms used by T[sub.reg] cells to suppress the immune system., Author(s): Anne O'Garra (corresponding author) [1]; Paulo Vieira [2] T[sub.reg] cells may be defined as CD4[sup.+] T cells that inhibit immunopathology or autoimmune disease in vivo. Specifically, T[sub.reg] cells include [...]

Published
2004
Full Text
View/download PDF

145. SOCS-3 regulates onset and maintenance of TH2-mediated allergic responses

Author

Seki, Yoh-ichi, Inoue, Hiromasa, Nagata, Naoko, Hayashi, Katsuhiko, Fukuyama, Satoru, Matsumoto, Koichiro, Komine, Okiru, Hamano, Shinjiro, Himeno, Kunisuke, Inagaki-Ohara, Kyoko, Cacalano, Nicholas, O'Garra, Anne, Oshida, Tadahilo, Saito, Hirohisa, Johnston, James A, Yoshimura, Akihiko, and Kubo, Masato

Abstract

Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (T[sub.H]2) cells, but its role in T[sub.H]2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased T[sub.H]2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased T[sub.H]2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T[sub.H]2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs., Author(s): Yoh-ichi Seki [1, 10]; Hiromasa Inoue [2, 10]; Naoko Nagata [3]; Katsuhiko Hayashi [1]; Satoru Fukuyama [2]; Koichiro Matsumoto [2]; Okiru Komine [1]; Shinjiro Hamano [4]; Kunisuke Himeno [4]; [...]

Published
2003
Full Text
View/download PDF

146. In vivo Manipulation of Dendritic Cell Migration and Activation to Elicit Antitumour Immunity

Author

Vicari, Alain P., primary, Vanbervliet, Béatrice, additional, Massacrier, Catherine, additional, Chiodoni, Claudia, additional, Vaure, Céline, additional, Aït-Yahia, Smina, additional, Dercamp, Christophe, additional, Matsos, Fabien, additional, Reynard, Olivier, additional, Taverne, Catherine, additional, Merle, Philippe, additional, Colombo, Mario P., additional, O'Garra, Anne, additional, Trinchieri, Giorgio, additional, and Caux, Christophe, additional

Published
2008
Full Text
View/download PDF

149. Development of a Fixed Repertoire of Blood Transcriptome Modules Based on Co-expression Patterns Across Immunological States

Author

Altman, Matthew, primary, Rinchai, Darawan, additional, Baldwin, Nicole, additional, Toufiq, Mohammed, additional, Whalen, Elizabeth, additional, Garand, Mathieu, additional, Kabeer, Basirudeen, additional, Alfaki, Mohamed, additional, Presnell, Scott, additional, Khaenam, Prasong, additional, Ayllon-Benitez, Aaron, additional, Mougin, Fleur, additional, Thébault, Patricia, additional, chiche, Laurent, additional, Jourde-Chiche, Noemie, additional, Phillips, Theodore, additional, Klintmalm, Goran, additional, O'Garra, Anne, additional, Berry, Matthew, additional, Bloom, Chloe, additional, Wilkinson, Robert, additional, Graham, Christine, additional, Lipman, Marc, additional, Lertmemongkolchai, Ganjana, additional, Bedognetti, Davide, additional, Thiébaut, Rodolphe, additional, Kheradmand, Farrah, additional, Mejias, Asuncion, additional, Ramilo, Octavio, additional, Palucka, Karolina, additional, Pascual, Virginia, additional, Banchereau, Jacques, additional, and Chaussabel, Damien, additional

Published
2020
Full Text
View/download PDF

150. Pandemic peak SARS-CoV-2 infection and seroconversion rates in London frontline health-care workers

Author

Houlihan, Catherine F, primary, Vora, Nina, additional, Byrne, Thomas, additional, Lewer, Dan, additional, Kelly, Gavin, additional, Heaney, Judith, additional, Gandhi, Sonia, additional, Spyer, Moira J, additional, Beale, Rupert, additional, Cherepanov, Peter, additional, Moore, David, additional, Gilson, Richard, additional, Gamblin, Steve, additional, Kassiotis, George, additional, McCoy, Laura E, additional, Swanton, Charles, additional, Hayward, Andrew, additional, Nastouli, Eleni, additional, Aitken, Jim, additional, Allen, Zoe, additional, Ambler, Rachel, additional, Ambrose, Karen, additional, Ashton, Emma, additional, Avola, Alida, additional, Balakrishnan, Samutheswari, additional, Barns-Jenkins, Caitlin, additional, Barr, Genevieve, additional, Barrell, Sam, additional, Basu, Souradeep, additional, Beesley, Clare, additional, Bhardwaj, Nisha, additional, Bibi, Shahnaz, additional, Bineva-Todd, Ganka, additional, Biswas, Dhruva, additional, Blackman, Michael J, additional, Bonnet, Dominique, additional, Bowker, Faye, additional, Broncel, Malgorzata, additional, Brooks, Claire, additional, Buck, Michael D, additional, Buckton, Andrew, additional, Budd, Timothy, additional, Burrell, Alana, additional, Busby, Louise, additional, Bussi, Claudio, additional, Butterworth, Simon, additional, Byrne, Fiona, additional, Byrne, Richard, additional, Caidan, Simon, additional, Campbell, Joanna, additional, Canton, Johnathan, additional, Cardoso, Ana, additional, Carter, Nick, additional, Carvalho, Luiz, additional, Carzaniga, Raffaella, additional, Chandler, Natalie, additional, Chen, Qu, additional, Churchward, Laura, additional, Clark, Graham, additional, Clayton, Bobbi, additional, Cobolli Gigli, Clementina, additional, Collins, Zena, additional, Cottrell, Sally, additional, Crawford, Margaret, additional, Cubitt, Laura, additional, Cullup, Tom, additional, Davies, Heledd, additional, Davis, Patrick, additional, Davison, Dara, additional, D'Avola, Annalisa, additional, Dearing, Vicky, additional, Debaisieux, Solene, additional, Diaz-Romero, Monica, additional, Dibbs, Alison, additional, Diring, Jessica, additional, Driscoll, Paul C, additional, Earl, Christopher, additional, Edwards, Amelia, additional, Ekin, Chris, additional, Evangelopoulos, Dimitrios, additional, Faraway, Rupert, additional, Fearns, Antony, additional, Ferron, Aaron, additional, Fidanis, Efthymios, additional, Fitz, Dan, additional, Fleming, James, additional, Frederico, Bruno, additional, Gaiba, Alessandra, additional, Gait, Anthony, additional, Gaul, Liam, additional, Golding, Helen M, additional, Goldman, Jacki, additional, Goldstone, Robert, additional, Gomez Dominguez, Belen, additional, Gong, Hui, additional, Grant, Paul R, additional, Greco, Maria, additional, Grobler, Mariana, additional, Guedan, Anabel, additional, Gutierrez, Maximiliano G, additional, Hackett, Fiona, additional, Hall, Ross, additional, Halldorsson, Steinar, additional, Harris, Suzanne, additional, Hashim, Sugera, additional, Healy, Lyn, additional, Herbst, Susanne, additional, Hewitt, Graeme, additional, Higgins, Theresa, additional, Hindmarsh, Steve, additional, Hirani, Rajnika, additional, Hope, Joshua, additional, Horton, Elizabeth, additional, Hoskins, Beth, additional, Houlihan, Catherine F, additional, Howell, Michael, additional, Howitt, Louise, additional, Hoyle, Jacqueline, additional, Htun, Mint R, additional, Hubank, Michael, additional, Huerga Encabo, Hector, additional, Hughes, Deborah, additional, Hughes, Jane, additional, Huseynova, Almaz, additional, Hwang, Ming-Shih, additional, Instrell, Rachael, additional, Jackson, Deborah, additional, Jamal-Hanjani, Mariam, additional, Jenkins, Lucy, additional, Jiang, Ming, additional, Johnson, Mark, additional, Jones, Leigh, additional, Kanu, Nnennaya, additional, Kiely, Louise, additional, King Spert Teixeira, Anastacio, additional, Kirk, Stuart, additional, Kjaer, Svend, additional, Knuepfer, Ellen, additional, Komarov, Nikita, additional, Kotzampaltiris, Paul, additional, Kousis, Konstantinos, additional, Krylova, Tammy, additional, Kucharska, Ania, additional, Labrum, Robyn, additional, Lambe, Catherine, additional, Lappin, Michelle, additional, Lee, Stacey-Ann, additional, Levett, Andrew, additional, Levett, Lisa, additional, Levi, Marcel, additional, Liu, Hon-Wing, additional, Loughlin, Sam, additional, Lu, Wei-Ting, additional, MacRae, James I, additional, Madoo, Akshay, additional, Marczak, Julie A, additional, Martensson, Mimmi, additional, Martinez, Thomas, additional, Marzook, Bishara, additional, Matthews, John, additional, Matz, Joachim M, additional, McCall, Samuel, additional, McKay, Fiona, additional, McNamara, Edel C, additional, Minutti, Carlos M, additional, Mistry, Gita, additional, Molina-Arcas, Miriam, additional, Montaner, Beatriz, additional, Montgomery, Kylie, additional, Moore, Catherine, additional, Moraiti, Anastasia, additional, Moreira-Teixeira, Lucia, additional, Mukherjee, Joyita, additional, Naceur-Lombardelli, Cristina, additional, Nelson, Aileen, additional, Nicod, Jerome, additional, Nightingale, Luke, additional, Nofal, Stephanie, additional, Nurse, Paul, additional, Nutan, Savita, additional, Oedekoven, Caroline, additional, O'Garra, Anne, additional, O'Leary, Jean D, additional, Olsen, Jessica, additional, O'Neill, Olga, additional, Ordonez Suarez, Paula, additional, O'Reilly, Nicola, additional, Osborne, Neil, additional, Pabari, Amar, additional, Pajak, Aleksandra, additional, Papayannopoulos, Venizelos, additional, Patel, Namita, additional, Patel, Yogen, additional, Paun, Oana, additional, Peat, Nigel, additional, Peces-Barba Castano, Laura, additional, Perez Caballero, Ana, additional, Perez-Lloret, Jimena, additional, Perrault, Magali S, additional, Perrin, Abigail, additional, Poh, Roy, additional, Poirier, Enzo Z, additional, Polke, James M, additional, Pollitt, Marc, additional, Prieto-Godino, Lucia, additional, Proust, Alize, additional, Shah Punatar, Rajvee, additional, Puvirajasinghe, Clinda, additional, Queval, Christophe, additional, Ramachandran, Vijaya, additional, Ramaprasad, Abhinay, additional, Ratcliffe, Peter, additional, Reed, Laura, additional, Reis e Sousa, Caetano, additional, Richardson, Kayleigh, additional, Ridewood, Sophie, additional, Roberts, Rowenna, additional, Rodgers, Angela, additional, Romero Clavijo, Pablo, additional, Rosa, Annachiara, additional, Rossi, Alice, additional, Roustan, Chloe, additional, Rowan, Andrew, additional, Sahai, Erik, additional, Sait, Aaron, additional, Sala, Katarzyna, additional, Sanderson, Theo, additional, Santucci, Pierre, additional, Sardar, Fatima, additional, Sateriale, Adam, additional, Saunders, Jill A, additional, Sawyer, Chelsea, additional, Schlott, Anja, additional, Schweighoffer, Edina, additional, Segura-Bayona, Sandra, additional, Shaw, Joe, additional, Shin, Gee Yen, additional, Silva Dos Santos, Mariana, additional, Silvestre, Margaux, additional, Singer, Matthew, additional, Snell, Daniel M, additional, Song, Ok-Ryul, additional, Steel, Louisa, additional, Strange, Amy, additional, Sullivan, Adrienne E, additional, Tan, Michele SY, additional, Tautz-Davis, Zoe H, additional, Taylor, Effie, additional, Taylor, Gunes, additional, Taylor, Harriet B, additional, Taylor-Beadling, Alison, additional, Teixeira Subtil, Fernanda, additional, Terré Torras, Berta, additional, Toolan-Kerr, Patrick, additional, Torelli, Francesca, additional, Toteva, Tea, additional, Treeck, Moritz, additional, Trojer, Hadija, additional, Tsai, Ming-Han C, additional, Turner, James MA, additional, Turner, Melanie, additional, Ule, Jernej, additional, Ulferts, Rachel, additional, Vanloo, Sharon P, additional, Veeriah, Selvaraju, additional, Venkatesan, Subramanian, additional, Vousden, Karen, additional, Wack, Andreas, additional, Walder, Claire, additional, Walker, Philip A, additional, Wang, Yiran, additional, Ward, Sophia, additional, Wenman, Catharina, additional, Wiliams, Luke, additional, Williams, Matthew J, additional, Wong, Wai Keong, additional, Wright, Joshua, additional, Wu, Mary, additional, Wynne, Lauren, additional, Xiang, Zheng, additional, Yap, Melvyn, additional, Zagalak, Julian A, additional, Zecchin, Davide, additional, Zillwood, Rachel, additional, Matthews, Rebecca, additional, Severn, Abigail, additional, Adam, Sajida, additional, Enfield, Louise, additional, McBride, Angela, additional, Gärtner, Kathleen, additional, Edwards, Sarah, additional, Lorencatto, Fabiana, additional, Michie, Susan, additional, Manley, Ed, additional, Shahmanesh, Maryam, additional, Lukha, Hinal, additional, Prymas, Paulina, additional, McBain, Hazel, additional, Shortman, Robert, additional, Wood, Leigh, additional, Davies, Claudia, additional, Williams, Bethany, additional, Ng, Kevin W, additional, Cornish, Georgina H, additional, Faulkner, Nikhil, additional, Riddell, Andrew, additional, Hobson, Philip, additional, Agua-Doce, Ana, additional, Bartolovic, Kerol, additional, Russell, Emma, additional, Carr, Lotte, additional, Sanchez, Emilie, additional, Frampton, Daniel, additional, Byott, Matthew, additional, Paraskevopoulou, Stavroula M, additional, Crayton, Elise, additional, Meyer, Carly, additional, Gkouleli, Triantafylia, additional, Stoltenberg, Andrea, additional, Ranieri, Veronica, additional, Byrne, Tom, additional, Roberts, Fiona, additional, and Hatipoglu, Emine, additional

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results