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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Inhibition of Th1 development mediated by GATA-3 through an IL-4-independent mechanism. Ouyang, W., Ranganath, S.H., Weindel, K., Bhattacharya, D., Murphy, T.L., Sha, W.C., Murphy, K.M. Immunity (1998) [Pubmed]
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