Autoimmunity to two forms of glutamate decarboxylase in insulin-dependent diabetes mellitus.

D L Kaufman; M G Erlander; M Clare-Salzler; M A Atkinson; N K Maclaren; A J Tobin

doi:10.1172/JCI115573

Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Department of Psychiatry and Behavioral Sciences, University of California Los Angeles 90024.

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Published in Volume 89, Issue 1 on January 1, 1992
J Clin Invest. 1992;89(1):283–292. https://doi.org/10.1172/JCI115573.
© 1992 The American Society for Clinical Investigation

Published January 1, 1992 - Version history

Insulin-dependent diabetes mellitus (IDDM) is thought to result from the autoimmune destruction of the insulin-producing beta cells of the pancreas. Years before IDDM symptoms appear, we can detect autoantibodies to one or both forms of glutamate decarboxylase (GAD65 and GAD67), synthesized from their respective cDNAs in a bacterial expression system. Individual IDDM sera show distinctive profiles of epitope recognition, suggesting different humoral immune responses. Although the level of GAD autoantibodies generally decline after IDDM onset, patients with IDDM-associated neuropathies have high levels of antibodies to GAD, years after the appearance of clinical IDDM. We note a striking sequence similarity between the two GADs and Coxsackievirus, a virus that has been associated with IDDM both in humans and in experimental animals. This similarity suggests that molecular mimicry may play a role in the pathogenesis of IDDM.

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