| Literature DB >> 15041039 |
Zandong Yang1, Meng Chen, Justin D Ellett, Lawrence B Fialkow, Jeffrey D Carter, Marcia McDuffie, Jerry L Nadler.
Abstract
Signal transducers and activators of transcription (STAT) proteins are activated in response to many cytokines, growth factors and hormones. STAT4 mediates IL-12 signaling and regulates T helper 1 (Th1) cell differentiation. Both IL-12 and Th1 cell activation participate in the development of autoimmune diabetes. In this study, we investigated the role of STAT4 in autoimmune diabetes. We crossbred Stat4 deficient (Stat4-/-) mice with nonobese diabetic (NOD) mice to generate the Stat4-/- NOD model. In Stat4-/- NOD mice, serum levels of both IFN-gamma and IL-2 were significantly reduced as compared to the controls. Insulin secretion in pancreatic islets was preserved in Stat4-/- NOD mice. Significantly, disruption of Stat4 activation completely prevented the development of spontaneous diabetes in NOD mice. This study reveals the important role of STAT4 in autoimmune diabetes pathogenesis.Entities:
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Year: 2004 PMID： 15041039 DOI： 10.1016/j.jaut.2003.08.006
Source DB: PubMed Journal: J Autoimmun ISSN： 0896-8411 Impact factor: 7.094