| First Author | Ouyang W | Year | 2000 |
| Journal | Immunity | Volume | 12 |
| Issue | 1 | Pages | 27-37 |
| PubMed ID | 10661403 | Mgi Jnum | J:331599 |
| Mgi Id | MGI:7388697 | Doi | 10.1016/s1074-7613(00)80156-9 |
| Citation | Ouyang W, et al. (2000) Stat6-independent GATA-3 autoactivation directs IL-4-independent Th2 development and commitment. Immunity 12(1):27-37 |
| abstractText | The initial source of IL-4-inducing Th2 development and the mechanism of stable Th2 commitment remain obscure. 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. |
