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The kinase ITK controls a Ca<sup>2+</sup>-mediated switch that balances T<sub>H</sub>17 and T<sub>reg</sub> cell differentiation.


ABSTRACT: The balance of proinflammatory T helper type 17 (TH17) and anti-inflammatory T regulatory (Treg) cells is crucial for immune homeostasis in health and disease. The differentiation of naïve CD4+ T cells into TH17 and Treg cells depends on T cell receptor (TCR) signaling mediated, in part, by interleukin-2-inducible T cell kinase (ITK), which stimulates mitogen-activated protein kinases (MAPKs) and Ca2+ signaling. Here, we report that, in the absence of ITK activity, naïve murine CD4+ T cells cultured under TH17-inducing conditions expressed the Treg transcription factor Foxp3 and did not develop into TH17 cells. Furthermore, ITK inhibition in vivo during allergic inflammation increa

SUBMITTER: Anannya O 

PROVIDER: S-EPMC11445781 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature