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• W1541097619 endingPage "2794" @default.
• W1541097619 startingPage "2786" @default.
• W1541097619 abstract "Inflammation can have both positive and negative effects on development of CD8 T cell memory, but the relative contributions and cellular targets of the cytokines involved are unclear. Using CD8 T cells lacking receptors for IL-12, type I IFN, or both, we show that these cytokines act directly on CD8 T cells to support memory formation in response to vaccinia virus and Listeria monocytogenes infections. Development of memory to vaccinia is supported predominantly by IL-12, whereas both IL-12 and type I IFN contribute to memory formation in response to Listeria. In contrast to memory formation, the inability to respond to IL-12 or type I IFN had a relatively small impact on the level of primary expansion, with at most a 3-fold reduction in the case of responses to Listeria. We further show that programming for memory development by IL-12 is complete within 3 days of the initial naive CD8 T cell response to Ag. This programming does not result in formation of a population that expresses killer cell lectin-like receptor G1, and the majority of the resulting memory cells have a CD62L(high) phenotype characteristic of central memory cells. Consistent with this, the cells undergo strong expansion upon rechallenge and provide protective immunity. These data demonstrate that IL-12 and type I IFN play an essential early role in determining whether Ag encounter by naive CD8 T cells results in formation of a protective memory population." @default.
• W1541097619 created "2016-06-24" @default.
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• W1541097619 date "2009-02-20" @default.
• W1541097619 modified "2023-10-11" @default.
• W1541097619 title "Programming for CD8 T Cell Memory Development Requires IL-12 or Type I IFN" @default.
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• W1541097619 doi "https://doi.org/10.4049/jimmunol.0803484" @default.
• W1541097619 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2648124" @default.
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