| First Author | Baker RL | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 1 | Pages | 39-43 |
| PubMed ID | 26608914 | Mgi Jnum | J:251651 |
| Mgi Id | MGI:6102423 | Doi | 10.4049/jimmunol.1501190 |
| Citation | Baker RL, et al. (2016) Cutting Edge: Nonobese Diabetic Mice Deficient in Chromogranin A Are Protected from Autoimmune Diabetes. J Immunol 196(1):39-43 |
| abstractText | T cells reactive to beta cell Ags are critical players in the development of autoimmune type 1 diabetes. Using a panel of diabetogenic CD4 T cell clones derived from the NOD mouse, we recently identified the beta cell secretory granule protein, chromogranin A (ChgA), as a new autoantigen in type 1 diabetes. CD4 T cells reactive to ChgA are pathogenic and rapidly transfer diabetes into young NOD recipients. We report in this article that NOD.ChgA(-/-) mice do not develop diabetes and show little evidence of autoimmunity in the pancreatic islets. Using tetramer analysis, we demonstrate that ChgA-reactive T cells are present in these mice but remain naive. In contrast, in NOD.ChgA(+/+) mice, a majority of the ChgA-reactive T cells are Ag experienced. Our results suggest that the presence of ChgA and subsequent activation of ChgA-reactive T cells are essential for the initiation and development of autoimmune diabetes in NOD mice. |
