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- W4313354857 abstract "Abstract Type 1 interferons (IFN), the first cytokines to be discovered, have been shown to regulate many aspects of the immune system. Type 1 IFN can act directly on CD8 T cells as a “signal 3” cytokine, which augments proliferation and differentiation of T cells into effectors in response to antigen. Exposure of CD8 T cells to IFN-inducers at the same time as antigen had stimulatory effects, whereas pre-exposure to IFN-inducers was inhibitory, indicating that the timing of IFN exposure was of essence. Pre-exposure of CD8 T cells to the type 1 IFN inducer and TLR agonist poly(I:C) had transient inhibitory effects on CD8 T cell proliferation. CD8 T cells lacking type 1 IFN receptors were resistant to the suppressive effects of poly(I:C), indicating a direct involvement of IFN. Poly(I:C)-pretreated CD8 T cells were refractory to further IFNβ stimulation, as measured by phosphorylation of STAT molecules, including STAT1, 3, 4, and 5. Reduced phospho-STAT levels were not due to a decrease in total STAT protein. Poly(I:C)-pretreated CD8 T cells phosphorylated STAT molecules in response to other cytokines, including IL-6 and IL-15. A decrease in type 1 IFN receptors and increased expression of SOCS1 likely contribute to the unresponsiveness to IFNβ stimulation. These data suggest that IFN-pretreated CD8 T cells are unable to get the positive effects that type 1 IFN provides as a “signal 3” cytokine, and this may partially explain why vaccines function poorly in virus-infected individuals." @default.
- W4313354857 created "2023-01-06" @default.
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- W4313354857 date "2013-05-01" @default.
- W4313354857 modified "2023-10-14" @default.
- W4313354857 title "Out of sequence “signal 3” suppresses CD8 T cell proliferation (P6040)" @default.
- W4313354857 doi "https://doi.org/10.4049/jimmunol.190.supp.49.3" @default.
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