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212. Additional file 2 of Hippocampal interleukin-33 mediates neuroinflammation-induced cognitive impairments

Author

Reverchon, Flora, Vidian De Concini, Larrigaldie, Vanessa, Benmerzoug, Sulayman, Briault, Sylvain, Dieudonnée Togbé, Ryffel, Bernhard, Quesniaux, Valérie F. J., and Menuet, Arnaud

Abstract

Additional file 2. Expression of IL-1a mRNA in hippocampi at 24 h and 48 h post-surgery, in Sham, vehicle or IL-33 intra-hippocampal treated mice with or without minocycline pretreatment. mRNA expression of the pro-inflammatory marker IL-1a was quantified in hippocampi by RT-qPCR normalized against 18S RNA. Relative fold change in vehicle group (grey bar) and in IL-33 group (black bar) were quantified versus sham group (S ; white bar). Minocycline treated mice were also analyzed at 48 h post-surgery (dotted bar). IL-33 injection delayed the resolution of inflammation highlighted by an increase of this markers at 48 h administration. A partial reduction of this effect was observed under minocycline exposure. Data are represented as mean ± SEM (n = 4-6). Statistical comparisons were made using Kruskal-Wallis followed by Dunn’s multiple comparison test for each group vs. Sham.**p ≤ 0.01, ***p ≤ 0.001. In addition, comparison between rmIL-33 (48 h) and rmIL-33 + mino (48 h) groups was performed using the Mann-Whithney test.

Published
2020
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213. Additional file 1 of Hippocampal interleukin-33 mediates neuroinflammation-induced cognitive impairments

Author

Reverchon, Flora, Vidian De Concini, Larrigaldie, Vanessa, Benmerzoug, Sulayman, Briault, Sylvain, Dieudonnée Togbé, Ryffel, Bernhard, Quesniaux, Valérie F. J., and Menuet, Arnaud

Abstract

Additional file 1. The emotional state of mice was tested 24H after the intrahippocampal microinjection. Anxiety-like behavior, representing by the time spent in center of the open field, was not different between: (a) mice intrahippocampal injected with vehicle solution (Veh) versus rmIL-33, (b) mice intrahippocampal injected with vehicle solution versus rmIL-33 treated with minocycline, (c) IL-1αβ KO mice intrahippocampal injected with vehicle solution versus rmIL-33. Values are mean ± SEM, n = 8-15 per group, Mann-Whitney test was used to compare the time spent in the center between 2 groups.

Published
2020
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221. NLRP3 inflammasome suppression improves longevity and prevents cardiac aging in male mice

Author

Junta de Andalucía, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Educación, Cultura y Deporte (España), Ministerio de Economía y Competitividad (España), Comunidad de Madrid, Marín-Aguilar, Fabiola, Lechuga-Vieco, Ana V., Alcocer-Gómez, Elísabet, Castejón-Vega, Beatriz, Lucas, Javier, Garrido, Carlos, Peralta‐Garcia, Alejandro, Pérez-Pulido, Antonio J., Varela‐López, Alfonso, Quiles, José Luis, Ryffel, Bernhard, Flores, Ignacio, Bullón, Pedro, Ruiz-Cabello, Jesús, Cordero, Mario D., Junta de Andalucía, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Educación, Cultura y Deporte (España), Ministerio de Economía y Competitividad (España), Comunidad de Madrid, Marín-Aguilar, Fabiola, Lechuga-Vieco, Ana V., Alcocer-Gómez, Elísabet, Castejón-Vega, Beatriz, Lucas, Javier, Garrido, Carlos, Peralta‐Garcia, Alejandro, Pérez-Pulido, Antonio J., Varela‐López, Alfonso, Quiles, José Luis, Ryffel, Bernhard, Flores, Ignacio, Bullón, Pedro, Ruiz-Cabello, Jesús, and Cordero, Mario D.

Abstract

While NLRP3‐inflammasome has been implicated in cardiovascular diseases, its role in physiological cardiac aging is largely unknown. During aging, many alterations occur in the organism, which are associated with progressive impairment of metabolic pathways related to insulin resistance, autophagy dysfunction, and inflammation. Here, we investigated the molecular mechanisms through which NLRP3 inhibition may attenuate cardiac aging. Ablation of NLRP3‐inflammasome protected mice from age‐related increased insulin sensitivity, reduced IGF‐1 and leptin/adiponectin ratio levels, and reduced cardiac damage with protection of the prolongation of the age‐dependent PR interval, which is associated with atrial fibrillation by cardiovascular aging and reduced telomere shortening. Furthermore, old NLRP3 KO mice showed an inhibition of the PI3K/AKT/mTOR pathway and autophagy improvement, compared with old wild mice and preserved Nampt‐mediated NAD+ levels with increased SIRT1 protein expression. These findings suggest that suppression of NLRP3 prevented many age‐associated changes in the heart, preserved cardiac function of aged mice and increased lifespan.

Published
2020

234. MyD88 is crucial for the development of a protective CNS immune response to Toxoplasma gondii infection

Author

Torres Marbel, Guiton Rachel, Lacroix-Lamandé Sonia, Ryffel Bernhard, Leman Samuel, and Dimier-Poisson Isabelle

Subjects
MyD88, innate immunity, Toxoplasma gondii, BALB/c mice, encephalitis, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Toxoplasmosis is one of the most common parasitic infections in humans. It can establish chronic infection and is characterized by the formation of tissue cysts in the brain. The cysts remain largely quiescent for the life of the host, but can reactivate and cause life-threatening toxoplasmic encephalitis in immunocompromised patients, such as those with AIDS, neoplastic diseases and organ transplants. Toll-like receptor (TLR) adaptor MyD88 activation is required for the innate sensing of Toxoplasma gondii. Mice deficient in MyD88 have defective IL-12 and Th1 effector responses, and are highly susceptible to the acute phase of T. gondii infection. However, the role of this signaling pathway during cerebral infection is poorly understood and requires examination. Method MyD88-deficient mice and control mice were orally infected with T. gondii cysts. Cellular and parasite infiltration in the peripheral organs and in the brain were determined by histology and immunohistochemistry. Cytokine levels were determined by ELISA and chemokine mRNA levels were quantified by real-time PCR (qPCR). Results Thirteen days after infection, a higher parasite burden was observed but there was no histological change in the liver, heart, lungs and small intestine of MyD88−/− and MyD88+/+ mice. However, MyD88−/− mice compared to MyD88+/+ mice were highly susceptible to cerebral infection, displayed high parasite migration to the brain, severe neuropathological signs of encephalitis and succumbed within 2 weeks of oral infection. Susceptibility was primarily associated with lower expression of Th1 cytokines, especially IL-12, IFN-γ and TNF-α, significant decrease in the expression of CCL3, CCL5, CCL7 and CCL19 chemokines, marked defect of CD8+ T cells, and infiltration of CD11b+ and F4/80+ cells in the brain. Conclusion MyD88 is essential for the protection of mice during the cerebral installation of T. gondii infection. These results establish a role for MyD88 in T cell-mediated control of T. gondii in the central nervous system (CNS).

Published
2013
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238. Transmembrane TNF and Partially TNFR1 Regulate TNFR2 Expression and Control Inflammation in Mycobacterial-Induced Pleurisy

Author

Uysal, Husnu, Chavez-Galan, Leslie, Vesin, Dominique, Blaser, Guillaume, Benkhoucha, Mahdia, Ryffel, Bernhard, Quesniaux, Valérie F. J., Garcia, Irene, Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Department of Pathology and Immunology, Univ. Geneva, and University of Geneva [Switzerland]

Subjects
Mice, Knockout, Pleural Cavity, BCG-induced pleurisy, Tumor Necrosis Factor-alpha, [SDV]Life Sciences [q-bio], TNF, Tuberculosis, Pleural, Mycobacterium bovis, Article, Receptors, Tumor Necrosis Factor, Mice, Inbred C57BL, lcsh:Chemistry, Disease Models, Animal, Mice, lcsh:Biology (General), lcsh:QD1-999, inflammation, Animals, Cytokines, Humans, [SDV.IMM]Life Sciences [q-bio]/Immunology, TNF receptors, lcsh:QH301-705.5, ComputingMilieux_MISCELLANEOUS
Abstract

Pleural tuberculosis is one of the most frequent forms of extra-pulmonary tuberculosis observed in patients infected with Mycobacterium tuberculosis. Tumor Necrosis Factor (TNF) is a crucial cytokine needed to control tuberculosis infection that remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may increase the risk of reactivation of latent infection resulting in overt pulmonary, pleural and extra-pulmonary tuberculosis. While TNF signaling is mainly considered pro-inflammatory, its requirement for the anti-inflammation process involved in the resolution of infection and tissue repair is less explored. Our study analyzes the role of TNF and TNF receptors in the control of the inflammatory process associated with Bacillus Calmette-Gu&eacute, rin (BCG)-induced pleurisy. This study shows that the absence of TNF causes exacerbated inflammation in the pleural cavity of BCG-infected mice which is controlled by the transmembrane TNF (tmTNF) expression. The lack of TNF is associated with an impaired cellular expression and shedding of TNFR2 in the pleural cavity. The presence of tmTNF restores the normal expression of TNFR2 on myeloid cells during BCG-induced pleurisy. We also show that absence of TNFR1 affects the expression of TNFR2 on pleural cells and inflammation in the pleural cavity of BCG-infected mice. In conclusion, tmTNF but not soluble TNF prevents pleural cavity inflammation leading to attenuation and the resolution of the inflammatory process caused by mycobacterial pleurisy in association with the expression of TNFR2 on myeloid cells.

Published
2018
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239. The cGAS/STING Pathway Is Important for Dendritic Cell Activation but Is Not Essential to Induce Protective Immunity against Mycobacterium tuberculosis Infection

Author

Marinho, Fabio V., Benmerzoug, Sulayman, Rose, Stéphanie, Campos, Priscila C., Marques, João T., Báfica, André, Barber, Glen, Ryffel, Bernhard, Oliveira, Sergio C., Quesniaux, Valérie, Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), and Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO)

Subjects
[SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018
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240. Interleukin‐23 promotes intestinal T helper type17 immunity and ameliorates obesity‐associated metabolic syndrome in a murine high‐fat diet model

Author

Martins, Larissa M S, Perez, Malena M, Pereira, Camila A, Costa, Frederico R C, Dias, Murilo S, Tostes, Rita C, Ramos, Simone G, de Zoete, Marcel R, Ryffel, Bernhard, Silva, João S, Carlos, Daniela, LS Infectiebiologie (Bacteriologie), dI&I I&I-2, Universidade de Brasilia [Brasília] (UnB), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Instituto de Engenharia de Sistemas e Computadores Investigação e Desenvolvimento em Lisboa (INESC-ID), Instituto Superior Técnico, Universidade Técnica de Lisboa (IST)-Instituto de Engenharia de Sistemas e Computadores (INESC), Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, and Universidade de São Paulo (USP)

Subjects
0301 basic medicine, medicine.medical_specialty, obesity, Receptor expression, [SDV]Life Sciences [q-bio], Immunology, Ileum, OBESIDADE, Biology, Gut flora, interleukin-17-producing T helper lymphocytes, 03 medical and health sciences, Insulin resistance, Intestinal mucosa, Internal medicine, medicine, Immunology and Allergy, Mesenteric lymph nodes, ComputingMilieux_MISCELLANEOUS, 2. Zero hunger, gut microbiota, digestive, oral, and skin physiology, food and beverages, nutritional and metabolic diseases, Original Articles, medicine.disease, biology.organism_classification, metabolic disease, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, inflammation, Steatosis, Metabolic syndrome, interleulin-23
Abstract

We addressed the role of interleukin-23 (IL-23) in driving the intestinal T helper type 17 (Th17) response during obesity and metabolic syndrome progression induced by a high-fat diet (HFD). Diet-induced obese and lean mice received HFD or control diet (CTD), respectively, for 20 weeks. The nutritional, metabolic and immune parameters were examined at weeks 9 and 20. Gene and protein IL-23p19 and IL-23 receptor expression was increased in the ileum of obese wild-type mice (WT) fed the HFD for 9 weeks. Mice lacking IL-23 and fed the HFD exhibited greater weight gain, higher fat accumulation, adipocyte hypertrophy and hepatic steatosis. Notably, these mice had more glucose intolerance, insulin resistance and associated metabolic alterations, such as hyperinsulinaemia and hyperlipidaemia. IL-23 deficiency also significantly reduced protein levels of IL-17, CCL20 and neutrophil elastase in the ileum and reduced Th17 cell expansion in the mesenteric lymph nodes of the HFD mice. Of importance, IL-23-deficient mice exhibited increased gut permeability and blood bacterial translocation compared with WT mice fed HFD. Finally, metagenomics analysis of gut microbiota revealed a dramatic outgrowth of Bacteroidetes over Firmicutes phylum with the prevalence of Bacteroides genera in the faeces of IL-23-deficient mice after HFD. In summary, IL-23 appears to maintain the Th17 response and neutrophil migration into the intestinal mucosa, minimizing the gut dysbiosis and protecting against obesity and metabolic disease development in mice.

Published
2018
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241. Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation

Author

Michaudel, Chloé, Maillet, Isabelle, Fauconnier, Louis, Quesniaux, Valérie, Chung, Kian Fan, Wiegman, Coen, Peter, Daniel, Ryffel, Bernhard, Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Artimmune SAS, Airway Disease Section, National Heart and Lung Institute, Imperial College London, Faculty of Informatics [Lugano], and Università della Svizzera italiana = University of Italian Switzerland (USI)

Subjects
Inflammation, Receptors, Interleukin-1 Type I, interleukin-1β, [SDV]Life Sciences [q-bio], interleukin-1α, epithelial cell, Immunology, Cell Differentiation, interleukin-18, Epithelium, myeloid differentiation factor-88, Mice, Inbred C57BL, ozone, Mice, Interleukin-1alpha, Myeloid Differentiation Factor 88, [SDV.IMM]Life Sciences [q-bio]/Immunology, Animals, Immunology and Allergy, Female, Lung, ComputingMilieux_MISCELLANEOUS, Original Research, Signal Transduction
Abstract

Air pollution associated with ozone exposure represents a major inducer of respiratory disease in man. In mice, a single ozone exposure causes lung injury with disruption of the respiratory barrier and inflammation. We investigated the role of interleukin-1 (IL-1)-associated cytokines upon a single ozone exposure (1 ppm for 1 h) using IL-1α-, IL-1β-, and IL-18-deficient mice or an anti-IL-1α neutralizing antibody underlying the rapid epithelial cell death. Here, we demonstrate the release of the alarmin IL-1α after ozone exposure and that the acute respiratory barrier injury and inflammation and airway hyperreactivity are IL-1α-dependent. IL-1α signaling via IL-1R1 depends on the adaptor protein myeloid differentiation factor-88 (MyD88). Importantly, epithelial cell signaling is critical, since deletion of MyD88 in lung type I alveolar epithelial cells reduced ozone-induced inflammation. In addition, intratracheal injection of recombinant rmIL-1α in MyD88acid mice led to reduction of inflammation in comparison with wild type mice treated with rmIL-1α. Therefore, a major part of inflammation is mediated by IL-1α signaling in epithelial cells. In conclusion, the alarmin IL-1α released upon ozone-induced tissue damage and inflammation is mediated by MyD88 signaling in epithelial cells. Therefore, IL-1α may represent a therapeutic target to attenuate ozone-induced lung inflammation and hyperreactivity.

Published
2018
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242. PD-1/PD-L1 pathway: an adaptive immune resistance mechanism to immunogenic chemotherapy in colorectal cancer

Author

Dosset, Magalie, Vargas, Thaiz Rivera, Lagrange, Anaïs, Boidot, Romain, Végran, Frédérique, Roussey, Aurélie, Chalmin, Fanny, Dondaine, Lucile, Paul, Catherine, Marie-Joseph, Elodie Lauret, Martin, François, Ryffel, Bernhard, Borg, Christophe, Adotévi, Olivier, Ghiringhelli, François, Apetoh, Lionel, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (HOTE GREFFON), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Université de Franche-Comté (UFC), Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer (LabEx LipSTIC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Université de Franche-Comté (UFC)-Université de Montpellier (UM), Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL), University of Cape Town, Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Service d'Oncologie Médicale [CHRU Besançon], Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Université de Franche-Comté (UFC), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Montpellier (UM), Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER, Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université, Plateforme de transfert en biologie cancérologique [Dijon], Centre d'épidémiologie des populations (CEP), Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER, Equipe CADIR (LNC - U1231), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL), ERT Géomatériaux, Géosciences Environnement Toulouse (GET), Centre National d'Études Spatiales [Toulouse] (CNES)-Observatoire Midi-Pyrénées (OMP), Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Météo France-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Observatoire Midi-Pyrénées (OMP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS)-Institut national des sciences de l'Univers (INSU - CNRS), Département d'oncologie médicale [Centre Georges-François Leclerc], Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), and UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-Université de Montpellier (UM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC)

Subjects
lcsh:Immunologic diseases. Allergy, [SDV]Life Sciences [q-bio], CD8 T cells, colorectal cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, chemotherapy, lcsh:RC254-282, digestive system diseases, cd8 t cells, colorectal cancer, adaptive immune resistance, immunotherapy, PD-1/PD-L1 pathway, lcsh:RC581-607, adaptive immune resistance, ComputingMilieux_MISCELLANEOUS, Original Research
Abstract

IF 5.503 (2017); International audience; Background: Chemotherapy is currently evaluated in order to enhance the efficacy of immune checkpoint blockade (ICB) therapy in colorectal cancer. However, the mechanisms by which these drugs could synergize with ICB remains unclear. The impact of chemotherapy on the PD-1/PD-L1 pathway and the resulting anticancer immune responses was assessed in two mouse models of colorectal cancer and validated in tumor samples from metastatic colorectal cancer patients that received neoadjuvant treatment. We demonstrated that 5-Fluorouracil plus Oxaliplatin (Folfox) drove complete tumor cure in mice when combined to anti-PD-1 treatment, while each monotherapy failed. This synergistic effect relies on the ability of Folfox to induce tumor infiltration by activated PD-1+ CD8 T cells in a T-bet dependent manner. This effect was concomitantly associated to the expression of PD-L1 on tumor cells driven by IFN-γ secreted by PD-1+ CD8 T cells, indicating that Folfox triggers tumor adaptive immune resistance. Finally, we observed an induction of PD-L1 expression and high CD8 T cell infiltration in the tumor microenvironment of colorectal cancer patients treated by Folfox regimen. Our study delineates a molecular pathway involved in Folfox-induced adaptive immune resistance in colorectal cancer. The results strongly support the use of immune checkpoint blockade therapy in combination with chemotherapies like Folfox.

Published
2018
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243. The alternative cap-binding complex is required for antiviral defense in vivo

Author

Gebhardt, Anna, primary, Bergant, Valter, additional, Schnepf, Daniel, additional, Moser, Markus, additional, Meiler, Arno, additional, Togbe, Dieudonnée, additional, Mackowiak, Claire, additional, Reinert, Line S., additional, Paludan, Søren R., additional, Ryffel, Bernhard, additional, Stukalov, Alexey, additional, Staeheli, Peter, additional, and Pichlmair, Andreas, additional

Published
2019
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244. Muc5b-deficient mice develop early histological lung abnormalities

Author

Valque, Hélène, primary, Gouyer, Valérie, additional, Duez, Catherine, additional, Leboeuf, Christophe, additional, Marquillies, Philippe, additional, Le Bert, Marc, additional, Plet, Ségolène, additional, Ryffel, Bernhard, additional, Janin, Anne, additional, Gottrand, Frédéric, additional, and Desseyn, Jean-Luc, additional

Published
2019
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246. NLRP3 inflammasome suppression improves longevity and prevents cardiac aging in male mice

Author

Marín‐Aguilar, Fabiola, primary, Lechuga‐Vieco, Ana V., additional, Alcocer‐Gómez, Elísabet, additional, Castejón‐Vega, Beatriz, additional, Lucas, Javier, additional, Garrido, Carlos, additional, Peralta‐Garcia, Alejandro, additional, Pérez‐Pulido, Antonio J., additional, Varela‐López, Alfonso, additional, Quiles, José L., additional, Ryffel, Bernhard, additional, Flores, Ignacio, additional, Bullón, Pedro, additional, Ruiz‐Cabello, Jesús, additional, and Cordero, Mario D., additional

Published
2019
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247. Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice

Author

Nascimento, Mégane, primary, Gombault, Aurélie, additional, Lacerda-Queiroz, Norinne, additional, Panek, Corinne, additional, Savigny, Florence, additional, Sbeity, Malak, additional, Bourinet, Manon, additional, Le Bert, Marc, additional, Riteau, Nicolas, additional, Ryffel, Bernhard, additional, Quesniaux, Valérie F. J., additional, and Couillin, Isabelle, additional

Published
2019
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248. NLRP3 Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPARα Activity

Author

Marín-Aguilar, Fabiola, primary, Castejón-Vega, Beatriz, primary, Alcocer-Gómez, Elísabet, primary, Lendines-Cordero, Debora, primary, Cooper, Matthew A, primary, de la Cruz, Patricia, primary, Andújar-Pulido, Eloísa, primary, Pérez-Alegre, Mónica, primary, Muntané, Jordi, primary, Pérez-Pulido, Antonio J, primary, Ryffel, Bernhard, primary, Robertson, Avril A B, primary, Ruiz-Cabello, Jesús, primary, Bullón, Pedro, primary, and Cordero, Mario D, primary

Published
2019
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250. Pre-conception maternal helminth infection transfers via nursing long-lasting cellular immunity against helminths to offspring

Author

Darby, Matthew G., primary, Chetty, Alisha, additional, Mrjden, Dunja, additional, Rolot, Marion, additional, Smith, Katherine, additional, Mackowiak, Claire, additional, Sedda, Delphine, additional, Nyangahu, Donald, additional, Jaspan, Heather, additional, Toellner, Kai-Michael, additional, Waisman, Ari, additional, Quesniaux, Valerie, additional, Ryffel, Bernhard, additional, Cunningham, Adam F., additional, Dewals, Benjamin G., additional, Brombacher, Frank, additional, and Horsnell, William G. C., additional

Published
2019
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