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- W2062131034 abstract "T helper 17 (Th17) cells play major roles in autoimmunity and bacterial infections, yet how T cell receptor (TCR) signaling affects Th17 cell differentiation is relatively unknown. We demonstrate that CD4+ T cells lacking Itk, a tyrosine kinase required for full TCR-induced phospholipase C-γ (PLC-γ1) activation, exhibit decreased interleukin-17A (IL-17A) expression in vitro and in vivo, despite relatively normal expression of retinoic acid receptor-related orphan receptor-γT (ROR-γT) and IL-17F. IL-17A expression was rescued by pharmacologically induced Ca2+ influx or constitutively activated nuclear factor of activated T cells (NFAT). Conversely, decreased TCR stimulation or calcineurin inhibition preferentially reduced IL-17A expression. We further found that the promoter of Il17a but not Il17f has a conserved NFAT binding site that bound NFATc1 in wild-type but not Itk-deficient cells, even though both exhibited open chromatin conformations. Finally, Itk−/− mice also showed differential regulation of IL-17A and IL-17F in vivo. Our results suggest that Itk specifically couples TCR signaling to Il17a expression and the differential regulation of Th17 cell cytokines through NFATc1." @default.
- W2062131034 created "2016-06-24" @default.
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- W2062131034 date "2009-10-01" @default.
- W2062131034 modified "2023-10-18" @default.
- W2062131034 title "Differential Expression of Interleukin-17A and -17F Is Coupled to T Cell Receptor Signaling via Inducible T Cell Kinase" @default.
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- W2062131034 doi "https://doi.org/10.1016/j.immuni.2009.07.009" @default.
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