Abstract
Insulin-dependent diabetes mellitus (IDDM) results from the T cell-mediated destruction of the insulin-producing β-cells. Intensive efforts have been directed towards understanding the events that trigger β-cell autoreactivity. Previous studies in an animal model of IDDM, the nonobese diabetic (NOD) mouse, have shown that T-cell reactivity first arises against glutamate decarboxylase (GAD) and then spreads to other β-cell antigens 1 Kaufman D.L. et al. Spontaneous loss of T-cell tolerance to glutamic acid decarboxylase in murine insulin-dependent diabetes. Nature. 1993; 366: 69-72 Crossref PubMed Scopus (1045) Google Scholar , 2 Tisch R. et al. Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice. Nature. 1993; 366: 72-75 Crossref PubMed Scopus (938) Google Scholar . The early inactivation of GAD-reactive T cells could prevent the development of autoreactivity, suggesting that the development of T-cell reactivity against GAD is key to the initiation and propagation of autoimmune responses against β-cells.
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