| First Author | Hwang SS | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 424 |
| Issue | 3 | Pages | 512-8 |
| PubMed ID | 22771806 | Mgi Jnum | J:186235 |
| Mgi Id | MGI:5431248 | Doi | 10.1016/j.bbrc.2012.06.146 |
| Citation | Hwang SS, et al. (2012) Aberrant expression of IFN-gamma in Th2 cells from Th2 LCR-deficient mice. Biochem Biophys Res Commun 424(3):512-8 |
| abstractText | The Th2 locus control region (LCR) has been shown to be a crucial cis-acting element for Th2 cytokine expression and Th2 cell differentiation. To study the role of Th2 LCR in ifng locus regulation, we examined the expression of IFN-gamma in Th2 cells from Th2 LCR-deficient mice. We found IFN-gamma to be aberrantly up-regulated. In addition, histone 3(H3)-acetylation and histone 3 lysine 4 (H3-K4)-methylation greatly increased at the ifng locus of the Th2 cells. GATA-3 and STAT6 bound to the ifng promoter in Th2 cells from the wild type but not from the Th2 LCR-deficient mice, and they directly repressed ifng expression in transient reporter assay. Moreover, ectopic expression of GATA-3 and STAT6-VT repressed the aberrant expression of the ifng gene and restored repressive chromatin state at the ifng locus in Th2 cells from Th2 LCR-deficient mice. These results suggest that expression of the ifng gene and chromatin remodeling of the ifng locus are under the control of a Th2 LCR-mediated Th2 differentiation program. |
