| First Author | Cain JA | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 3 | Pages | 1645-54 |
| PubMed ID | 16424194 | Mgi Jnum | J:126603 |
| Mgi Id | MGI:3761734 | Doi | 10.4049/jimmunol.176.3.1645 |
| Citation | Cain JA, et al. (2006) NKT cells and IFN-gamma establish the regulatory environment for the control of diabetogenic T cells in the nonobese diabetic mouse. J Immunol 176(3):1645-54 |
| abstractText | In type 1 diabetes mellitus (T1DM), T cell-mediated destruction of insulin-producing pancreatic beta cells leads to the acute onset of hyperglycemia. The nonobese diabetic mouse model of human T1DM reveals that T cells capable of inducing diabetes can escape normal central tolerance, and can cause T1DM if left unchecked. However, several regulatory T cell subsets can temper autoaggressive T cells, although it remains undetermined when and how, and by which subset, homeostatic control of diabetogenic T cells is normally achieved in vivo. Using a cotransfer model, we find that NKT cells efficiently dampen the action of diabetogenic CD4+ T cells, and do so in an indirect manner by modifying the host environment. Moreover, the NKT cell-containing population modifies the host via production of IFN-gamma that is necessary for driving the inhibition of diabetogenic T cells in vivo. |
