| First Author | Stassen M | Year | 2007 |
| Journal | Mol Immunol | Volume | 44 |
| Issue | 5 | Pages | 926-33 |
| PubMed ID | 16650898 | Mgi Jnum | J:113233 |
| Mgi Id | MGI:3664832 | Doi | 10.1016/j.molimm.2006.03.019 |
| Citation | Stassen M, et al. (2007) p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1. Mol Immunol 44(5):926-33 |
| abstractText | Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 is a target for p38 MAP kinase-mediated phosphorylation in vitro, we conclude that both signaling molecules represent a part of a mast cell-specific signaling network that regulates the expression of IL-9. |
