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CUTTING EDGE |
Responses in T Lymphocytes
* Division of Biological Sciences, and Cancer Center, University of California, San Diego, La Jolla, CA 92093; and
Biogen-Idec, Inc., Cambridge, MA 02142
Engagement of the IFN-
receptor initiates multiple signaling cascades, including activation of the STAT. In this study, we demonstrate that IFN-, although antiproliferative in wild-type CD4+ or CD8+ T cells, act as strong mitogens on their STAT1–/– counterparts. Furthermore, IFN- 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- 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- response, and support a model in which the IFN- receptor initiates both pro- and antiapoptotic responses through STAT1, and STAT3 and STAT5A/B, respectively.
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