Regulation of antiviral T cell responses by type I interferons

Key Points Type I interferons (IFNs) are pro-inflammatory cytokines that have an essential role during viral infections. Type I IFNs not only function as innate cytokines but are also involved in regulating antiviral T cell responses. Regulation of antiviral T cells by type I IFNs occurs through bot...

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Veröffentlicht in:Nature reviews. Immunology 2015-04, Vol.15 (4), p.231-242
Hauptverfasser: Crouse, Josh, Kalinke, Ulrich, Oxenius, Annette
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Sprache:eng
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Zusammenfassung:Key Points Type I interferons (IFNs) are pro-inflammatory cytokines that have an essential role during viral infections. Type I IFNs not only function as innate cytokines but are also involved in regulating antiviral T cell responses. Regulation of antiviral T cells by type I IFNs occurs through both direct signalling on T cells and indirect signalling through accessory cells. Indirect regulation of T cells by type I IFNs is mediated by both the innate antiviral functions of type I IFNs, and by the modulation of antigen-presenting cell function. Direct signalling of type I IFNs on T cells can have both augmenting and inhibitory effects, contingent on the timing of the signal relative to T cell receptor activation. Type I interferons (IFNs) have both direct and indirect effects on T cells, and can promote or inhibit their antiviral activity. As reviewed here, the outcome of type I IFN signalling in T cells largely depends on the timing of the signal relative to T cell receptor activation. Type I interferons (IFNs) are pro-inflammatory cytokines that are rapidly induced in different cell types during viral infections. The consequences of type I IFN signalling include direct antiviral activity, innate immune cell activation and regulation of adaptive immune responses. In this Review, we discuss recent conceptual advances in our understanding of indirect and direct regulation of T cell immunity by type I IFNs, which can either promote or inhibit T cell activation, proliferation, differentiation and survival. This regulation depends, to a large extent, on the timing of type I IFN exposure relative to T cell receptor signalling. Type I IFNs also provide activated T cells with resistance to natural killer cell-mediated elimination.
ISSN:1474-1733
1474-1741
DOI:10.1038/nri3806