Protein kinase C theta (PKCtheta) is essential for T cell activation, as it is 
required for the activation of NF-kappaB and expression of IL-2. PKCtheta has 
also been shown to affect NFAT activation and Th2 differentiation. To better 
understand the role of PKCtheta in the regulation of T helper cells, we used 
PKCtheta-deficient DO11.10 transgenic T cells to study its role in vitro. 
DO11.10 Th1 cells deficient in PKCtheta produced significantly less TNF-alpha 
and IL-2. The expression of Th2 cytokines, including IL-4, IL-5, IL-10, IL-13 
and IL-24 was significantly reduced in PKCtheta-deficient T cells. Moreover, the 
expression of the Th2 transcription factor, GATA3, was significantly reduced in 
PKCtheta-deficient T cells. Overexpression of GATA3 by retroviral infection in 
PKCtheta-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 PKCtheta regulates Th2 cytokine expression via GATA3.