Following a diabetogenic T cell from genesis through pathogenesis

JD Katz, B Wang, K Haskins, C Benoist, D Mathis - Cell, 1993 - cell.com
JD Katz, B Wang, K Haskins, C Benoist, D Mathis
Cell, 1993cell.com
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 …
Abstract
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.
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