| First Author | Won HY | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 394 |
| Issue | 3 | Pages | 811-6 |
| PubMed ID | 20233578 | Mgi Jnum | J:159228 |
| Mgi Id | MGI:4442106 | Doi | 10.1016/j.bbrc.2010.03.079 |
| Citation | Won HY, et al. (2010) Galpha12 is critical for TCR-induced IL-2 production and differentiation of T helper 2 and T helper 17 cells. Biochem Biophys Res Commun 394(3):811-6 |
| abstractText | G12 family have been known to modulate a variety of cellular events such as cell migration, B cell activation and maturation, cytokine production, and cell differentiation. In particular, Galpha12 modulates IgG production, thus induces IgG antibody-mediated immune responses. However, it is largely unknown whether Galpha12 is required for T cell-mediated immune functions. In this study, we investigated the effects of Galpha12 in the activation and differentiation of CD4+ T cells. While PMA plus ionomycin induced equal levels of IL-2 production in WT and Galpha12-deficient lymphocytes, TCR-triggered IL-2 production was significantly attenuated in Galpha12 KO lymphocytes. In particular, CD4+ T cells and effector Th cells lacking of Galpha12 revealed diminished IL-2 production, but not IFNgamma production, upon TCR stimulation. In addition, supplement of IL-2 preferentially induced Galpha12-deficient CD4+ T cells into Th2 and Th17 cells; however, the expression of specific transcription factors was unchanged in Galpha12 KO Th cells. While IL-2 expression was still diminished by the re-stimulation with anti-CD3, PMA plus ionomycin restored IL-2 production in Galpha12-deficient Th1 and Th2 cells. These results suggest that Galpha12 may be a critical signaling molecule in TCR-induced IL-2 production and also relay a signal to suppress Th2 and Th17 cell differentiation. |
