دورية أكاديمية
Respiratory Syncytial Virus Infects Regulatory B Cells in Human Neonates via Chemokine Receptor CX3CR1 and Promotes Lung Disease Severity
| العنوان: | Respiratory Syncytial Virus Infects Regulatory B Cells in Human Neonates via Chemokine Receptor CX3CR1 and Promotes Lung Disease Severity |
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| المؤلفون: | Zhivaki, Dania, Lemoine, Sebastien, Lim, Annick, Morva, Ahsen, Vidalain, Pierre-Olivier, Schandene, Liliane, Casartelli, Nicoletta, Rameix-Welti, Marie-Anne, Herve, Pierre Louis, Deriaud, Edith, Beitz, Benoit, Ripaux-Lefevre, Maryline, Miatello, Jordi, Lemercier, Brigitte, Lorin, Valerie, Descamps, Delphyne, Fix, Jenna, Eleouet, Jean Francois, Riffault, Sabine, Schwartz, Olivier, Porcheray, Fabrice, Mascart, Francoise, Mouquet, Hugo, Zhang, Xiaoming, Tissieres, Pierre, Lo-Man, Richard |
| المساهمون: | Histopathologie humaine et Modèles animaux, Institut Pasteur Paris (IP), Université Paris Diderot - Paris 7 (UPD7), Régulation Immunitaire et Vaccinologie, Institut Pasteur Paris (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Département d'Immunologie - Department of Immunology, Génomique virale et vaccination, Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS), Immunobiology Clinic, Hôpital Erasme Bruxelles (ULB), Faculté de Médecine Bruxelles (ULB), Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB)-Faculté de Médecine Bruxelles (ULB), Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB), Virus et Immunité - Virus and immunity (CNRS-UMR3569), Infection et inflammation (2I), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Laboratoire de Microbiologie, Hôpital Raymond Poincareé, Unité de recherche Virologie et Immunologie Moléculaires (VIM (UR 0892)), Institut National de la Recherche Agronomique (INRA), Université Paris-Saclay, Microbiology Technology Institute, BIOASTER Microbiology Technology Institute Lyon, School of Medicine, University of Patras, Physiologie et physiopathologie des rétrovirus endogènes et infectieux (RETRO-ENDO), Institut Gustave Roussy (IGR)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS), APHP, Pediatric ICU and Neonatal Medicine, Hôpitaux Universitaires Paris Sud AP-HP (HUPS), Réponse humorale aux pathogènes, Institut Pasteur Paris (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Vaccinology and Mucosal Immunity, Université libre de Bruxelles (ULB), Institut Pasteur de Shanghai, Académie des Sciences de Chine - Chinese Academy of Sciences (IPS-CAS), Réseau International des Instituts Pasteur (RIIP), This work was supported by an ANR grant (ANR 13-BSV3-0016) and by the Fondation pour la Recherche Médicale (grant no. DEQ20120323719). This study also received funding from the French Government’s Investissement d’Avenir program, Laboratoire d’Excellence “Integrative Biology of Emerging Infectious Diseases” (grant no. ANR-10-LABX-62-IBEID). X.Z. and S.L. were supported by ANR and by the European Commission FP7 ADITEC program (HEALTH-F4-2011-280873). X.Z. was also partially supported by the Major Basic Research Project of Shanghai Science and Technology Commission (no. 13JC1405600), National Natural Science Foundation of China (31270961, 31470879), Interdisciplinary Innovation Team and External Cooperation Program (no. GJHZ201312), and Chinese Academy of Sciences. D.Z. was supported by DIM Malinf of Region IdF. Work in the O.S. lab is also supported by ANRS, Sidaction and Fondation Areva. We acknowledge the Center for Human Immunology at Institut Pasteur for support in conducting these studies., We are very grateful to T. Domet (Therapie Cellulaire, Hopital Saint-Louis) for the cord blood sample collection and M. Lucas-Hourani for some viral preparation. We thank F. Huetz for helpful discussion about B lymphocytes., ANR-13-BSV3-0016,SyncBreg,Signature moléculaire et fonction des lymphocytes B régulateurs dans l'infection VRS(2013), ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 280873,EC:FP7:HEALTH,FP7-HEALTH-2011-single-stage,ADITEC(2011) |
| المصدر: | ISSN: 1074-7613 ; Immunity ; https://hal.science/hal-01604975Test ; Immunity, 2017, 46 (2), pp.301-314. ⟨10.1016/j.immuni.2017.01.010⟩. |
| بيانات النشر: | HAL CCSD Elsevier |
| سنة النشر: | 2017 |
| المجموعة: | Université de Versailles Saint-Quentin-en-Yvelines: HAL-UVSQ |
| مصطلحات موضوعية: | Breg cell, bronchiolitis, newborn, respiratory syncytial virus, [SDV]Life Sciences [q-bio], [SDV.IMM]Life Sciences [q-bio]/Immunology |
| الوصف: | International audience ; Respiratory syncytial virus (RSV) is the major cause of lower respiratory tract infections in infants and is characterized by pulmonary infiltration of B cells in fatal cases. We analyzed the B cell compartment in human newborns and identified a population of neonatal regulatory B lymphocytes (nBreg cells) that produced interleukin 10 (IL-10) in response to RSV infection. The polyreactive B cell receptor of nBreg cells interacted with RSV protein F and induced upregulation of chemokine receptor CX3CR1. CX3CR1 interacted with RSV glycoprotein G, leading to nBreg cell infection and IL-10 production that dampened T helper 1 (Th1) cytokine production. In the respiratory tract of neonates with severe RSV-induced acute bronchiolitis, RSV-infected nBreg cell frequencies correlated with increased viral load and decreased blood memory Th1 cell frequencies. Thus, the frequency of nBreg cells is predictive of the severity of acute bronchiolitis disease and nBreg cell activity may constitute an early-life host response that favors microbial pathogenesis. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/28228284; info:eu-repo/grantAgreement/EC/FP7/280873/EU/Advanced Immunization Technologies/ADITEC; hal-01604975; https://hal.science/hal-01604975Test; PRODINRA: 391675; PUBMED: 28228284; PUBMEDCENTRAL: PMC7128247; WOS: 000396410900017 |
| DOI: | 10.1016/j.immuni.2017.01.010 |
| الإتاحة: | https://doi.org/10.1016/j.immuni.2017.01.010Test https://hal.science/hal-01604975Test |
| رقم الانضمام: | edsbas.B2BDF655 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1016/j.immuni.2017.01.010 |
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