Abstract：
:Stat6 is critical for IL-4-mediated Th2 cell development, but its molecular mechanism remains unclear. Here we constructed Stat6:ER, a Stat6-estrogen receptor fusion protein that can be activated by 4-hydroxy-tamoxifen, independently of IL-4 and endogenous Stat6. Retrovirus-mediated introduction of Stat6:ER into developing Th1 cells induced Th2-specific cytokines and suppressed IFNgamma production in a 4-HT-dependent manner and in the absence of IL-4. It also induced GATA-3 and c-maf expression and downregulated IL-12Rbeta2 chain expression. Its decreased ability to induce the Th2 phenotype with progressing Th1 cell commitment correlated with a decreased induction of GATA-3 and c-maf. This study indicates that Stat6 functions upstream of GATA-3 and c-Maf to induce Th2 development.
journal_name
Immunityjournal_title
Immunityauthors
Kurata H,Lee HJ,O'Garra A,Arai Ndoi
10.1016/s1074-7613(00)80142-9keywords:
subject
Has Abstractpub_date
1999-12-01 00:00:00pages
677-88issue
6eissn
1074-7613issn
1097-4180pii
S1074-7613(00)80142-9journal_volume
11pub_type
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