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21 results on '"McNab, Finlay W"'

4. Investigation of Janus Kinase (JAK) Inhibitors for Lung Delivery and the Importance of Aldehyde Oxidase Metabolism

Author

Wellaway, Christopher R., primary, Baldwin, Ian R., additional, Bamborough, Paul, additional, Barker, Daniel, additional, Bartholomew, Michelle A., additional, Chung, Chun-wa, additional, Dümpelfeld, Birgit, additional, Evans, John P., additional, Fazakerley, Neal J., additional, Homes, Paul, additional, Keeling, Steven P., additional, Lewell, Xiao Q., additional, McNab, Finlay W., additional, Morley, Joanne, additional, Needham, Deborah, additional, Neu, Margarete, additional, van Oosterhout, Antoon J. M., additional, Pal, Anshu, additional, Reinhard, Friedrich B. M., additional, Rianjongdee, Francesco, additional, Robertson, Craig M., additional, Rowland, Paul, additional, Shah, Rishi R., additional, Sherriff, Emma B., additional, Sloan, Lisa A., additional, Teague, Simon, additional, Thomas, Daniel A., additional, Wellaway, Natalie, additional, Wojno-Picon, Justyna, additional, Woolven, James M., additional, and Coe, Diane M., additional

Published
2021
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5. 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
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6. Diverse cytokine production by NKT cell subsets and identification of an IL-17-producing [CD4.sup.-][NK1.1.sup.-] NKT cell population

Author

Coquet, Jonathan M., Chakravarti, Sumone, Kyparissoudis, Konstantinos, McNab, Finlay W., Pitt, Lauren A., McKenzie, Brent S., Berzins, Stuart P., Smyth, Mark J., and Godfrey, Dale I.

Subjects
T cells -- Properties, Cytokines -- Physiological aspects, Science and technology
Abstract

NKT cell subsets can be divided based on CD4 and NK1.1 expression and tissue of origin, but the developmental and functional relationships between the different subsets still are poorly understood. A comprehensive study of 19 cytokines across different NKT cell subsets revealed that no two NKT subpopulations exhibited the same cytokine profile, and, remarkably, the amounts of each cytokine produced varied by up to 100-fold or more among subsets. This study also revealed the existence of a population of C[D4.sup.-]N[K1.1-sup.-]NKT cells that produce high levels of the pro-inflammatory cytokine IL-17 within 2-3 h of activation. On intrathymic transfer these cells develop into mature CD4-N[K1.1.-sup.+] but not into CD4+N[K1.1.-sup.+] NKT cells, indicating that CD4-N[K1.1.-sup.-] NKT cells include an IL-17-producing subpopulation, and also mark the elusive branch point for C[D4.sup.+] and C[D4.sup.-] NKT cell sublineages. cytokines | CDld | thymus | Tcell

Published
2008

7. Investigation of Janus Kinase (JAK) Inhibitors for Lung Delivery and the Importance of Aldehyde Oxidase Metabolism.

Author

Wellaway, Christopher R., Baldwin, Ian R., Bamborough, Paul, Barker, Daniel, Bartholomew, Michelle A., Chun-wa Chung, Dümpelfeld, Birgit, Evans, John P., Fazakerley, Neal J., Homes, Paul, Keeling, Steven P., Lewell, Xiao Q., McNab, Finlay W., Morley, Joanne, Needham, Deborah, Neu, Margarete, van Oosterhout, Antoon J. M., Pal, Anshu, Reinhard, Friedrich B. M., and Rianjongdee, Francesco

Published
2022
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9. Type I IFN Inhibits Alternative Macrophage Activation during Mycobacterium tuberculosis Infection and Leads to Enhanced Protection in the Absence of IFN-γ Signaling

Author

Moreira-Teixeira, Lúcia, primary, Sousa, Jeremy, additional, McNab, Finlay W., additional, Torrado, Egídio, additional, Cardoso, Filipa, additional, Machado, Henrique, additional, Castro, Flávia, additional, Cardoso, Vânia, additional, Gaifem, Joana, additional, Wu, Xuemei, additional, Appelberg, Rui, additional, Castro, António Gil, additional, O’Garra, Anne, additional, and Saraiva, Margarida, additional

Published
2016
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10. Analysis of Transcriptional Signatures in Response to Listeria monocytogenes Infection Reveals Temporal Changes That Result from Type I Interferon Signaling

Author

Pitt, Jonathan M., primary, Blankley, Simon, additional, Potempa, Krzysztof, additional, Graham, Christine M., additional, Moreira-Teixeira, Lucia, additional, McNab, Finlay W., additional, Howes, Ashleigh, additional, Stavropoulos, Evangelos, additional, Pascual, Virginia, additional, Banchereau, Jacques, additional, Chaussabel, Damien, additional, and O’Garra, Anne, additional

Published
2016
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11. Type I IFN Induces IL-10 Production in an IL-27–Independent Manner and Blocks Responsiveness to IFN-γ for Production of IL-12 and Bacterial Killing in Mycobacterium tuberculosis–Infected Macrophages

Author

McNab, Finlay W., primary, Ewbank, John, additional, Howes, Ashleigh, additional, Moreira-Teixeira, Lucia, additional, Martirosyan, Anna, additional, Ghilardi, Nico, additional, Saraiva, Margarida, additional, and O’Garra, Anne, additional

Published
2014
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12. TPL-2–ERK1/2 Signaling Promotes Host Resistance against Intracellular Bacterial Infection by Negative Regulation of Type I IFN Production

Author

McNab, Finlay W., primary, Ewbank, John, additional, Rajsbaum, Ricardo, additional, Stavropoulos, Evangelos, additional, Martirosyan, Anna, additional, Redford, Paul S., additional, Wu, Xuemei, additional, Graham, Christine M., additional, Saraiva, Margarida, additional, Tsichlis, Philip, additional, Chaussabel, Damien, additional, Ley, Steven C., additional, and O’Garra, Anne, additional

Published
2013
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14. The Immune Response in Tuberculosis

Author

O'Garra, Anne, primary, Redford, Paul S., additional, McNab, Finlay W., additional, Bloom, Chloe I., additional, Wilkinson, Robert J., additional, and Berry, Matthew P.R., additional

Published
2013
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16. Programmed death ligand 1 is over-expressed by neutrophils in the blood of patients with active tuberculosis

Author

McNab, Finlay W., primary, Berry, Matthew P. R., additional, Graham, Christine M., additional, Bloch, Susannah A. A., additional, Oni, Tolu, additional, Wilkinson, Katalin A., additional, Wilkinson, Robert J., additional, Kon, Onn M., additional, Banchereau, Jacques, additional, Chaussabel, Damien, additional, and O'Garra, Anne, additional

Published
2011
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21. Diverse cytokine production by NKT cell subsets and identification of an IL-17—producing CD4-NK1.1- NKT cell population.

Author

Coquet, Jonathan M., Chakravarti, Sumone, Kyparissoudis, Konstantinos, McNab, Finlay W., Pitt, Lauren A., McKenzie, Brent S., Berzins, Stuart P., Smyth, Mark J., and Godfrey, Dale I.

Subjects
CELLULAR immunity, CELL proliferation, CELLS, CYTOKINES, IMMUNOREGULATION
Abstract

NKT cell subsets can be divided based on CD4 and NK1.1 expression and tissue of origin, but the developmental and functional relationships between the different subsets still are poorly understood. A comprehensive study of 19 cytokines across different NKT cell subsets revealed that no two NKT subpopulations exhibited the same cytokine profile, and, remarkably, the amounts of each cytokine produced varied by up to 100-fold or more among subsets. This study also revealed the existence of a population of CD4-NK1.1- NKT cells that produce high levels of the proinflammatory cytokine IL-17 within 2-3 h of activation. On intrathymic transfer these cells develop into mature CD4-NK1.1+ but not into CD4+NK1.1+ NKT cells, indicating that CD4-NK1.1- NKT cells include an IL-17-producing subpopulation, and also mark the elusive branch point for CD4+ and CD4- NKT cell sublineages. [ABSTRACT FROM AUTHOR]

Published
2008
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