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Publication : Inhibition of Th1 development mediated by GATA-3 through an IL-4-independent mechanism.

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.
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