| First Author | Tanaka Y | Year | 2005 |
| Journal | Blood | Volume | 106 |
| Issue | 4 | Pages | 1286-95 |
| PubMed ID | 15845902 | Mgi Jnum | J:117328 |
| Mgi Id | MGI:3696001 | Doi | 10.1182/blood-2004-10-4074 |
| Citation | Tanaka Y, et al. (2005) Impaired IL-4 and c-Maf expression and enhanced Th1-cell development in Vav1-deficient mice. Blood 106(4):1286-95 |
| abstractText | Although c-Maf is crucial for Th2 differentiation and production of interleukin 4 (IL-4), its regulation is poorly understood. We report that Vav1-/- CD4+ T cells display deficient T-cell receptor (TCR)/CD28-induced IL-4 and c-Maf expression and, conversely, enhanced interferon gamma (IFN-gamma) production and T-bet expression (even when cultured under Th2-polarizing conditions), but intact expression of other Th2 cytokines and GATA-3. Up-regulation of c-Maf was dependent on Ca2+/nuclear factor of activated T cell (NFAT) and, together with IL-4 production, could be rescued in Vav1-/- T cells by Ca2+ ionophore. Deficient IL-4 production was restored by retrovirus-mediated Vav1 expression, but only partially by retroviral c-Maf expression. Similar IL-4 --> IFN-gamma skewing was observed in intact, antigen-primed Vav1-/- mice. Thus, Vav1 is selectively required for IL-4 and c-Maf expression, a requirement reflecting, at least in part, the dependence of c-Maf expression on Ca2+/NFAT signaling. |
