ITK signaling regulates a switch between T helper 17 and T regulatory cell lineages via a calcium-mediated pathway.

ABSTRACT: The balance of pro-inflammatory T helper type 17 (Th17) and anti-inflammatory T regulatory (Treg) cells is crucial in maintaining immune homeostasis in health and disease conditions. Differentiation of naïve CD4⁺ T cells into Th17/Treg cells is dependent upon T cell receptor (TCR) activation and cytokine signaling, which includes the kinase ITK. Signals from ITK can regulate the differentiation of Th17 and Treg cell fate choice, however, the mechanism remains to be fully understood. We report here that in the absence of ITK activity, instead of developing into Th17 cells under Th17 conditions, naïve CD4⁺ T cells switch to cells expressing the Treg marker Foxp3 (Forkhead box P3). These switched Foxp3⁺ Treg like cells retain suppressive function and resemble

SUBMITTER: Anannya O 

PROVIDER: S-EPMC10103963 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature