Involvement of GATA3 in Protein Kinase C θ‐induced Th2 cytokine expression

Abstract

Abstract Protein kinase C θ (PKCθ) is essential for T cell activation, as it is required for the activation of NF‐κB and expression of IL‐2. PKCθ has also been shown to affect NFAT activation and Th2 differentiation. To better understand the role of PKCθ in the regulation of T helper cells, we used PKCθ‐deficient DO11.10 transgenic T cells to study its role in vitro . DO11.10 Th1 cells deficient in PKCθ produced significantly less TNF‐α and IL‐2. The expression of Th2 cytokines, including IL‐4, IL‐5, IL‐10, IL‐13 and IL‐24 was significantly reduced in PKCθ‐deficient T cells. Moreover, the expression of the Th2 transcription factor, GATA3, was significantly reduced in PKCθ‐deficient T cells. Overexpression of GATA3 by retroviral infection in PKCθ‐deficient T cells resulted in increased expansion of IL‐4‐producing T cells and higher IL‐4 production than that of wild type Th2 cells. IL‐5, IL‐10, IL‐13 and IL‐24 expressions were also rescued by GATA3 overexpression. Our observations suggest that PKCθ regulates Th2 cytokine expression via GATA3.