| First Author | Goswami R | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 3 | Pages | 968-75 |
| PubMed ID | 22180613 | Mgi Jnum | J:180779 |
| Mgi Id | MGI:5307203 | Doi | 10.4049/jimmunol.1102840 |
| Citation | Goswami R, et al. (2012) STAT6-dependent regulation of Th9 development. J Immunol 188(3):968-75 |
| abstractText | Th cell effector subsets develop in response to specific cytokine environments. The development of a particular cytokine-secreting pattern requires an integration of signals that may promote the development of opposing pathways. A recent example of this paradigm is the IL-9-secreting Th9 cell that develops in response to TGF-beta and IL-4, cytokines that, in isolation, promote the development of inducible regulatory T cells and Th2 cells, respectively. To determine how the balance of these factors results in priming for IL-9 secretion, we examined the effects of each pathway on transcription factors that regulate Th cell differentiation. We demonstrated that TGF-beta induces the PU.1-encoding Sfpi1 locus and that this is independent of IL-4-induced STAT6 activation. IL-4-activated STAT6 is required for repressing the expression of T-bet and Foxp3 in Th9 cells, transcription factors that inhibit IL-9 production, and STAT6 is required for the induction of IRF4, which promotes Th9 development. These data established a transcription factor network that regulates IL-9 and demonstrated how combinations of cytokine signals generate cytokine-secreting potential by altering the expression of a panel of transcription factors. |
