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. 2000 Jan;12(1):27-37.
doi: 10.1016/s1074-7613(00)80156-9.

"V体育安卓版" Stat6-independent GATA-3 autoactivation directs IL-4-independent Th2 development and commitment

W Ouyang  1 , M Löhning, Z Gao, M Assenmacher, S Ranganath, A Radbruch, K M Murphy
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Stat6-independent GATA-3 autoactivation directs IL-4-independent Th2 development and commitment

W Ouyang et al. Immunity. 2000 Jan.
Free article

Abstract

The initial source of IL-4-inducing Th2 development and the mechanism of stable Th2 commitment remain obscure VSports手机版. We found the reduced level of IL-4 production in Stat6-deficient T cells to be significantly higher than in Th1 controls. Using a novel cell surface affinity matrix technique, we found that IL-4-secreting Stat6-deficient T cells stably expressed GATA-3 and Th2 phenotype. Introducing GATA-3 into Stat6-deficient T cells completely restored Th2 development, inducing c-Maf, Th2-specific DNase I hypersensitive sites in the IL-4 locus, and Th2 cytokine expression. The fact that GATA-3 fully reconstitutes Th2 development in Stat6-deficient T cells indicates it is a master switch in Th2 development. Finally, GATA-3 exerts Stat6-independent autoactivation, creating a feedback pathway stabilizing Th2 commitment. .

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