| First Author | Tanabe Y | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 2 | Pages | 609-13 |
| PubMed ID | 15634877 | Mgi Jnum | J:95845 |
| Mgi Id | MGI:3527393 | Doi | 10.4049/jimmunol.174.2.609 |
| Citation | Tanabe Y, et al. (2005) Cutting edge: role of STAT1, STAT3, and STAT5 in IFN-alphabeta responses in T lymphocytes. J Immunol 174(2):609-13 |
| abstractText | Engagement of the IFN-alphabeta receptor initiates multiple signaling cascades, including activation of the STAT. In this study, we demonstrate that IFN-alphabeta, although antiproliferative in wild-type CD4(+) or CD8(+) T cells, act as strong mitogens on their STAT1(-/-) counterparts. Furthermore, IFN-alphabeta exert little effect on apoptosis in wild-type cells, but are potent survival factors in the absence of STAT1. The antiapoptotic response in the absence of STAT1 is predominantly mediated by STAT3, and to a lesser extent by STAT5A/B. In contrast, the mitogenic IFN-alphabeta response gained through the absence of STAT1 is only marginally affected when STAT5A/B expression is also abrogated, but is completely dependent on STAT3 activation. These findings provide the first evidence for a function of STAT3 and STAT5A/B in the IFN-alphabeta response, and support a model in which the IFN-alphabeta receptor initiates both pro- and antiapoptotic responses through STAT1, and STAT3 and STAT5A/B, respectively. |
