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• W2025924171 abstract "Abstract We here investigate the crosstalk of PKC and PKA signaling during primary CD3+ T-lymphocyte activation using pharmacologic inhibitors and activators in combination with our established panel of PKC isotype–deficient mouse T cells in vitro. PKCθ and PKA inversely affect the CD3/CD28-induced IL-2 expression, whereas other PKC isotypes are dispensable in this signaling pathway. Gene ablation of PKCθ selectively results in a profound reduction of IL-2 production; however, complete abrogation of IL-2 production in these PKCθ–/– T cells was achieved only by simultaneous coactivation of the cAMP/PKA pathway in CD3+ T cells. Conversely, the reduced IL-2 production in PKC inhibitor–treated T cells can be rescued by inhibition of the cAMP/PKA pathway in wild-type but not in PKCθ–/– T cells. Mechanistically, the cAMP/PKA and PKCθ pathways converge at the level of NF-AT, as shown by DNA binding analysis. The combined increase in PKA and decrease in PKCθ activity leads to an enhanced inhibition of nuclear NF-AT translocation. This PKCθ/PKA crosstalk significantly affects neither the NF-κB, the AP-1, nor the CREB pathways. Taken together, this opposite effect between the positive PKCθ and the negative cAMP/PKA signaling pathways appears rate limiting for NF-AT transactivation and IL-2 secretion responses of CD3+ T lymphocytes." @default.
• W2025924171 created "2016-06-24" @default.
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• W2025924171 date "2006-06-15" @default.
• W2025924171 modified "2023-09-27" @default.
• W2025924171 title "PKCθ and PKA are antagonistic partners in the NF-AT transactivation pathway of primary mouse CD3+ T lymphocytes" @default.
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• W2025924171 doi "https://doi.org/10.1182/blood-2005-10-4044" @default.
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