Abstract
Diabetes in nonobese diabetic (NOD) mice is an autoimmune disease characterized by the destruction of the β cells in the pancreas. We have previously reported that transgenic expression of interleukin-4 (IL-4) counterregulates the disease process, completely protecting NOD mice from insulitis and diabetes. Here we demonstrate the presence of autoreactivity but lack of pathogenicity of the IL-4-regulated lymphocytes. The importance of T cell diversity for the protective effect of IL-4 is demonstrated through breeding with transgenic BDC2.5 mice, which have an almost exclusively monoclonal T cell repertoire. Limitation of T cell diversity abrogated the protection by IL-4. We suggest that 'immune deviation' in NOD-IL-4 mice is mediated by the pancreatic tissue itself, which causes activation of distinct, nonpathogenic T cell specificities.
Original language | English (US) |
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Pages (from-to) | 411-418 |
Number of pages | 8 |
Journal | Immunity |
Volume | 7 |
Issue number | 3 |
DOIs | |
State | Published - Sep 1997 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases