| First Author | Stevens L | Year | 2006 |
| Journal | Eur J Immunol | Volume | 36 |
| Issue | 12 | Pages | 3305-14 |
| PubMed ID | 17111354 | Mgi Jnum | J:117083 |
| Mgi Id | MGI:3695548 | Doi | 10.1002/eji.200636400 |
| Citation | Stevens L, et al. (2006) Involvement of GATA3 in protein kinase C theta-induced Th2 cytokine expression. Eur J Immunol 36(12):3305-14 |
| abstractText | 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. |
