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- W2306571638 abstract "Abstract NKT cells produce protective immune mediators at early stages of infections, preceding the responses of MHC-restricted T cells, and thus are thought a key bridge between innate and adaptive immune responses. Early IFNγ secretion by NKT cells during bacterial infections can result from autoantigenic activation with co-stimulation from IL-12&IL-18. However, the cellular processes underlying the rapid responsiveness of NKT cells remain poorly understood. Here we show that auto-antigenic stimulation of NKT cells potentiates them to secrete IFNγ in response to subsequent exposure to IL-12&IL-18. Rested NKT cells did not respond to IL-12&IL-18, however, NKT cells pre-exposed to CD1d+ APCs subsequently showed a transient ability to transcribe IFNγ mRNA and to secrete IFNγ protein in response to these cytokines without concurrent TCR stimulation. The potentiation effect was dependent on TCR signaling during pre-exposure. The subsequent cytokine response was p38 dependent and calcium signaling independent. The potentiation effect was transient, which distinguishes it from classical Th1 differentiation. The window of responsiveness was not due to regulation of cytokine receptor expression on NKT cells. Thus, we hypothesize that autoantigenic activation may induce epi-genetic changes in NKT cells that transiently confer an innate-like ability to respond to cytokines without concurrent TCR signaling." @default.
- W2306571638 created "2016-06-24" @default.
- W2306571638 creator A5074900624 @default.
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- W2306571638 date "2009-04-01" @default.
- W2306571638 modified "2023-09-27" @default.
- W2306571638 title "Auto-antigenic stimulation potentiates NKT cells for subsequent innate IFN-gamma secretion (134.23)" @default.
- W2306571638 doi "https://doi.org/10.4049/jimmunol.182.supp.134.23" @default.
- W2306571638 hasPublicationYear "2009" @default.
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