First Author | Ouyang W | Year | 1998 |
Journal | Immunity | Volume | 9 |
Issue | 5 | Pages | 745-55 |
PubMed ID | 9846495 | Mgi Jnum | J:51355 |
Mgi Id | MGI:1315135 | Doi | 10.1016/s1074-7613(00)80671-8 |
Citation | Ouyang W, et al. (1998) Inhibition of Th1 development mediated by GATA-3 through an IL-4-independent mechanism. Immunity 9(5):745-55 |
abstractText | Recently, the transcription factor GATA-3 was shown to be selectively expressed in Th2 but not Th1 cells and to augment Th2-specific cytokines. Here, we show that loss of GATA-3 expression by developing Th1 cells requires IL-12 signaling through Stat4 and does not simply result from an absence of IL-4. Moreover, we demonstrate a novel role for GATA-3 in directly repressing Th1 development distinct from its positive actions on Th2-specific cytokines. GATA-3 inhibits Th1 cytokines by a cell-intrinsic mechanism that is not dependent on IL-4 and that may involve repression of IL-12 signaling. Thus, GATA-3 expression and IL-12 signaling are mutually antagonistic, which facilitates rapid dominance of one pathway during early Th development, producing a stable divergence in cytokine profiles. |