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

Wenjun Ouyang, Sheila H. Ranganath, Kathryn Weindel, Deepta Bhattacharya, Theresa L. Murphy, William C. Sha, Kenneth M. Murphy

Research output: Contribution to journalArticlepeer-review

656 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)745-755
Number of pages11
JournalImmunity
Volume9
Issue number5
DOIs
StatePublished - Nov 1998

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