| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1933756 | Biochemical and Biophysical Research Communications | 2009 | 5 Pages |
STAT6 plays critical roles in Th2 cell differentiation, whereas STAT4 and T-bet are important for Th1 cell differentiation. However, it is still largely unknown about the cross talk of these transcription factors during Th1/Th2 cell differentiation. To further address the regulatory mechanisms underlying Th1/Th2 cell differentiation, we generated the mice lacking both STAT6 and T-bet (STAT6−/−T-bet−/− mice). Importantly, although Th2 cell differentiation was severely and similarly decreased in STAT6−/−T-bet−/− mice and STAT6−/− mice, Th1 cell differentiation was rescued in part in STAT6−/−T-bet−/− mice as compared with that in T-bet−/− mice. While no significant difference was observed in the expression of IL-12Rβ2 and STAT4 between STAT6−/−T-bet−/− CD4+ T cells and T-bet−/− CD4+ T cells, IL-12-induced STAT4 phosphorylation was increased in STAT6−/−T-bet−/− CD4+ T cells as compared with that in T-bet−/− CD4+ T cells. These results indicate that STAT6 inhibits T-bet-independent Th1 cell differentiation by suppressing IL-12-STAT4 signaling.
