First Author | Katz JD | Year | 1993 |
Journal | Cell | Volume | 74 |
Issue | 6 | Pages | 1089-100 |
PubMed ID | 8402882 | Mgi Jnum | J:77007 |
Mgi Id | MGI:2180888 | Doi | 10.1016/0092-8674(93)90730-e |
Citation | Katz JD, et al. (1993) Following a diabetogenic T cell from genesis through pathogenesis. Cell 74(6):1089-100 |
abstractText | Nonobese diabetic (NOD) mice spontaneously develop a disease very similar to type 1 diabetes in humans. We have generated a transgenic mouse strain carrying the rearranged T cell receptor genes from a diabetogenic T cell clone derived from a NOD mouse. Self-reactive T cells expressing the transgene-encoded specificity are not tolerized in these animals, resulting in rampant insulitis and eventually diabetes. Features of the disease process emphasize two so-called check-points, recognized previously in the NOD and human diseases but easily misinterpreted. Although NOD mice are protected from insulitis and diabetes by expression of the E molecule encoded in the major histocompatibility complex, the transgenics are not, permitting us to exclude some possible mechanisms of protection. |