| First Author | Zhao W | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 1 | Pages | 463-71 |
| PubMed ID | 17579067 | Mgi Jnum | J:149412 |
| Mgi Id | MGI:3848423 | Doi | 10.4049/jimmunol.179.1.463 |
| Citation | Zhao W, et al. (2007) Stat2-dependent regulation of MHC class II expression. J Immunol 179(1):463-71 |
| abstractText | MHC type II (MHC II) expression is tightly regulated in macrophages and potently induced by IFN-gamma (type II IFN). In contrast, type I IFNs (IFN-Is), which are far more widely expressed, fail to induce MHC II expression, even though both classes of IFNs direct target gene expression through Stat1. The unexpected finding that IFN-Is effectively induce MHC II expression in Stat2(-/-) macrophages provided an opportunity to explore this conundrum. The ensuing studies revealed that deletion of Stat2, which uniquely transduces signals for IFN-Is, leads to a loss in the IFN-I-dependent induction of suppressor of cytokine signaling-1. Impairment in the expression of this important negative regulator led to a striking prolongation in IFN-I-dependent Stat1 activation, as well as enhanced expression of the target gene, IFN-regulatory factor-1. The prolonged activity of these two transcription factors synergized to drive the transcription of CIITA, the master regulator of MHC II expression, analogous to the pattern observed in IFN-gamma-treated macrophages. Thus, IFN-I-dependent suppressor of cytokine signaling-1 expression plays an important role in distinguishing the biological response between type I and II IFNs in macrophages. |
