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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.
Volume 284, Number 5417, Issue of 14 May 1999,
p. 1085. Copyright © 1999 by The American Association for the
Advancement of Science. All rights reserved.
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