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• W2234504829 abstract "Inflammation can boost antigen-specific adaptive immune responses. Ziegler and colleagues show that type I interferon-mediated inflammation can also affect bystander naive CD4+ T cells by transiently increasing their expression of Foxp3, which might limit aggressive responses against self-antigens. Inflammation induced during infection can both promote and suppress immunity. This contradiction suggests that inflammatory cytokines affect the immune system in a context-dependent manner. Here we show that nonspecific bystander inflammation conditions naive CD4+ T cells for enhanced peripheral Foxp3 induction and reduced effector differentiation. This results in inhibition of immune responses in vivo via a Foxp3-dependent effect on antigen-specific naive CD4+ T cell precursors. Such conditioning may have evolved to allow immunity to infection while limiting subsequent autoimmunity caused by release of self-antigens in the wake of infection. Furthermore, this phenomenon suggests a mechanistic explanation for the idea that early tuning of the immune system by infection affects the long-term quality of immune regulation." @default.
• W2234504829 created "2016-06-24" @default.
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• W2234504829 date "2016-01-11" @default.
• W2234504829 modified "2023-10-13" @default.
• W2234504829 title "Conditioning of naive CD4+ T cells for enhanced peripheral Foxp3 induction by nonspecific bystander inflammation" @default.
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• W2234504829 doi "https://doi.org/10.1038/ni.3329" @default.
• W2234504829 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4757503" @default.
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