| First Author | Phillips JM | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 11 | Pages | 6087-91 |
| PubMed ID | 11714766 | Mgi Jnum | J:119045 |
| Mgi Id | MGI:3701046 | Doi | 10.4049/jimmunol.167.11.6087 |
| Citation | Phillips JM, et al. (2001) Cutting edge: interactions through the IL-10 receptor regulate autoimmune diabetes. J Immunol 167(11):6087-91 |
| abstractText | BDC2.5/nonobese diabetic (NOD) transgenic mice express a TCR from a diabetogenic T cell clone yet do not spontaneously develop diabetes at high incidence. Evidence exists showing that in the absence of endogenous TCR alpha-chain rearrangements this transgenic mouse spontaneously develops diabetes and that CTLA-4 negatively regulates diabetes onset. This strongly suggests that onset of diabetes in BDC2.5/NOD mice is governed by T cell regulation. We addressed the mechanism of immune regulation in BDC2.5/NOD mice. We find that activated spleen cells from young, but not old, BDC2.5/NOD mice are able to transfer diabetes to NOD-scid recipients. We have used anti-IL-10R to show that the failure of splenocytes from older mice to transfer diabetes is due to dominant regulation. We furthermore found that diabetes developed following anti-IL-10R treatment of 6-wk old BDC2.5/NOD mice indicating that endogenous IL-10 plays a key role in the regulation of diabetes onset in this transgenic mouse. |
