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Science 14 May 1999:
Vol. 284. no. 5417, p. 1085
DOI: 10.1126/science.284.5417.1085k
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In type I diabetes, the immune system destroys the insulin-producing b cells of the pancreas. T cells to specific antigens develop--those recognizing glutamic acid decarboxylase (GAD) appear early in disease. Transfer of these T cells to nondiabetic animals can initiate disease. Yoon et al. (p. 1183; see the Perspective by Boehmer and Sarukhan) report that expression of GAD in b cells is required for the development of diabetes in NOD mice, the mouse model of type I diabetes. A series of mice were developed that expressed increasing amounts of an antisense gene to GAD messenger RNA. When expression was high, little GAD was detected on the b cells, and the NOD mice did not develop diabetes. Transfer of b cells from these mice into diabetic NOD mice cured NOD diabetes. Thus, not only was GAD necessary for the development of diabetogenic T cells, but the b cells were not destroyed in mice with ongoing disease unless they expressed GAD.




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