| First Author | Li Q | Year | 2011 |
| Journal | Clin Immunol | Volume | 140 |
| Issue | 1 | Pages | 3-7 |
| PubMed ID | 21592863 | Mgi Jnum | J:172590 |
| Mgi Id | MGI:5008338 | Doi | 10.1016/j.clim.2011.04.010 |
| Citation | Li Q, et al. (2011) The role of interferon alpha in initiation of type I diabetes in the NOD mouse. Clin Immunol 140(1):3-7 |
| abstractText | Type 1 diabetes (T1D) is an autoimmune disease in both humans and the nonobese diabetic (NOD) mouse, in which the insulin-producing-cells of the pancreatic islets are destroyed by a beta islet cell-specific T cell immune response. We recently reported that interferon (IFN)-alpha is an early trigger of the T1D process in NOD mice. Here, we show that extensive blockade of IFN-alpha action by a monoclonal antibody specific to IFN-alpha receptor 1 results in nearly complete prevention of T1D in NOD mice. Whether professional IFN-alpha producing cells, plasmacytoid dendritic cells (pDCs), are responsible for the initiation of T1D has been unclear. Here we demonstrate that depletion of pDCs in NOD mice by a specific mAb given at 15-25days of age significantly delays the onset and decreases the incidence of T1D. These findings indicate that pDC and pDC-derived IFN-alpha are the prime initiators of the pathogenesis of T1D in NOD mice. |
