Ectopic expression of activated Stat6 induces the expression of Th2-specific cytokines and transcription factors in developing Th1 cells. NLM AIDSLINE Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

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Ectopic expression of activated Stat6 induces the expression of Th2-specific cytokines and transcription factors in developing Th1 cells.

Immunity. 1999 Dec;11(6):677-88. Unique Identifier : AIDSLINE MED/20090316
Kurata H; Lee HJ; O'Garra A; Arai N; Department of Immunobiology, DNAX Research Institute of Molecular; and Cellular Biology, Palo Alto, California 94304, USA.


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.


Keywords: JOURNAL ARTICLE Animal Binding Sites Cell Division Cytokines/BIOSYNTHESIS/*GENETICS DNA/METABOLISM DNA-Binding Proteins/GENETICS Gene Expression Regulation Genetic Vectors/GENETICS Interferon Type II/GENETICS/METABOLISM Interleukin-12/GENETICS Interleukin-4/IMMUNOLOGY/PHARMACOLOGY Mice Mice, Transgenic Proto-Oncogene Proteins/GENETICS Receptors, Estrogen/AGONISTS/GENETICS Recombinant Fusion Proteins/GENETICS Retroviridae/GENETICS Tamoxifen/ANALOGS & DERIVATIVES/PHARMACOLOGY Th1 Cells/DRUG EFFECTS/*METABOLISM Th2 Cells/DRUG EFFECTS/*IMMUNOLOGY Time Factors Trans-Activation (Genetics) Trans-Activators/GENETICS/*PHYSIOLOGY Transcription Factors/BIOSYNTHESIS/*GENETICS

KWDjournalarticleanimalbindingsitescelldivisioncytokines/biosynthesis/
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