IL-10 suppresses T cell expansion while promoting tissue-resident memory cell formation during SARS-CoV-2 infection in rhesus macaques.
Autor: | Nelson CE; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Foreman TW; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Fukutani ER; Laboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil., Kauffman KD; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Sakai S; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Fleegle JD; Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Gomez F; Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Gould ST; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Le Nouën C; RNA Viruses Section, Laboratory of Infectious Disease, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Liu X; RNA Viruses Section, Laboratory of Infectious Disease, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Burdette TL; SARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America., Garza NL; SARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America., Lafont BAP; SARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America., Brooks K; Barrier Immunity Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Lindestam Arlehamn CS; Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, United States of America., Weiskopf D; Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, United States of America., Sette A; Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, California, United States of America.; Department of Medicine, Division of Infectious Diseases and Global Public Health, University of California, San Diego (UCSD), La Jolla, California, United States of America., Hickman HD; Viral Immunity and Pathogenesis Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Buchholz UJ; RNA Viruses Section, Laboratory of Infectious Disease, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Johnson RF; SARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America., Brenchley JM; Barrier Immunity Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Oberman JP; Holy Cross Germantown Hospital, Affiliate of National Breathe Free Sinus and ENT Center, Frederick Breathe Free Sinus and ENT Center, Frederick, Maryland, United States of America., Quieroz ATL; Laboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil., Andrade BB; Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America., Via LE; Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.; Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.; Institute of Infectious Disease & Molecular Medicine and Division of Immunology, Department of Pathology, University of Cape Town, Observatory, South Africa., Barber DL; T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America. |
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Jazyk: | angličtina |
Zdroj: | PLoS pathogens [PLoS Pathog] 2024 Jul 01; Vol. 20 (7), pp. e1012339. Date of Electronic Publication: 2024 Jul 01 (Print Publication: 2024). |
DOI: | 10.1371/journal.ppat.1012339 |
Abstrakt: | The regulation of inflammatory responses and pulmonary disease during SARS-CoV-2 infection is incompletely understood. Here we examine the roles of the prototypic pro- and anti-inflammatory cytokines IFNγ and IL-10 using the rhesus macaque model of mild COVID-19. We find that IFNγ drives the development of 18fluorodeoxyglucose (FDG)-avid lesions in the lungs as measured by PET/CT imaging but is not required for suppression of viral replication. In contrast, IL-10 limits the duration of acute pulmonary lesions, serum markers of inflammation and the magnitude of virus-specific T cell expansion but does not impair viral clearance. We also show that IL-10 induces the subsequent differentiation of virus-specific effector T cells into CD69+CD103+ tissue resident memory cells (Trm) in the airways and maintains Trm cells in nasal mucosal surfaces, highlighting an unexpected role for IL-10 in promoting airway memory T cells during SARS-CoV-2 infection of macaques. Competing Interests: A.S. is a consultant for Gritstone Bio, Flow Pharma, Moderna, AstraZeneca, Qiagen, Avalia, Fortress, Gilead, Sanofi, Merck, RiverVest, MedaCorp, Turnstone, NA Vaccine Institute, Gerson Lehrman Group and Guggenheim. LJI has filed for patent protection for various aspects of T cell epitope and vaccine design work. All other authors have no competing interests to disclose. (Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.) |
Databáze: | MEDLINE |
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