PLoS pathogens · 2024
IL-10 suppresses T cell expansion while promoting tissue-resident memory cell formation during SARS-CoV-2 infection in rhesus macaques.
СтатьяResearch Support, N.I.H., IntramuralНазвание и аннотация: Перевод в очереди
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Nelson Christine E, Foreman Taylor W, Fukutani Eduardo R, Kauffman Keith D, Sakai Shunsuke, Fleegle Joel D, Gomez Felipe, NIAID/DIR Tuberculosis Imaging Program, Gould Sydnee T, Le Nouën Cyril, Liu Xueqiao, Burdette Tracey L, Garza Nicole L, Lafont Bernard A P, Brooks Kelsie, Lindestam Arlehamn Cecilia S, Weiskopf Daniela, Sette Alessandro, Hickman Heather D, Buchholz Ursula J, Johnson Reed F, Brenchley Jason M, Oberman James P, Quieroz Artur T L, Andrade Bruno B, Via Laura E, Barber Daniel L
Аннотация
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.