| First Author | Jaeckel E | Year | 2004 |
| Journal | Nat Immunol | Volume | 5 |
| Issue | 10 | Pages | 1028-35 |
| PubMed ID | 15378058 | Mgi Jnum | J:92693 |
| Mgi Id | MGI:3054307 | Doi | 10.1038/ni1120 |
| Citation | Jaeckel E, et al. (2004) Recessive tolerance to preproinsulin 2 reduces but does not abolish type 1 diabetes. Nat Immunol 5(10):1028-35 |
| abstractText | Although autoimmune diseases can be initiated by immunization with a single antigen, it is not clear whether a single self antigen is essential for the initiation and, perhaps, the perpetuation of spontaneous autoimmunity. Some studies have suggested that insulin may represent an essential autoantigen in type 1 diabetes. Here we show that unlike tolerance to glutamic acid decarboxylase, tolerance to transgenically overexpressed preproinsulin 2 substantially reduced the onset and severity of type 1 diabetes in nonobese diabetic mice. However, some mice still developed type 1 diabetes, suggesting that insulin is a key, but not absolutely essential, autoantigen. The results are consistent with the idea that the human IDDM2 locus controls susceptibility to type 1 diabetes by regulating intrathymic preproinsulin expression. |
