| First Author | Yang Z | Year | 2004 |
| Journal | J Autoimmun | Volume | 22 |
| Issue | 3 | Pages | 191-200 |
| PubMed ID | 15041039 | Mgi Jnum | J:90600 |
| Mgi Id | MGI:3044271 | Doi | 10.1016/j.jaut.2003.08.006 |
| Citation | Yang Z, et al. (2004) Autoimmune diabetes is blocked in Stat4-deficient mice. J Autoimmun 22(3):191-200 |
| abstractText | 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. |
