Glutamic acid decarboxylase--gene to antigen to disease

J Intern Med. 1996 Nov;240(5):259-77. doi: 10.1046/j.1365-2796.1996.27859000.x.

Abstract

Glutamic acid decarboxylase (GAD) enzymes catalyse the formation of gamma-aminobuturic acid (GABA), which is a major transmitter in the central nervous system but also exerts functions in peripheral organs. Recent-molecular analyses have revealed surprising new roles for the GAD isoforms in human diseases of autoimmune character including neurological disorders and insulin-dependent diabetes. In the 1995 Frontiers in Medicine Symposium, the co-authors of this review discussed the genetics, cell biology, molecular immunology and the role of GAD as autoantigens in human autoimmunity. Studies on disease diagnosis, prediction, and prognosis have revealed unique patterns of reactivities in both cellular and humoral immune responses. Further work will be needed to establish whether the GAD molecules can be used to treat autoimmune diseases.

Publication types

  • Review

MeSH terms

  • Animals
  • Autoantibodies / blood
  • Autoimmune Diseases / immunology*
  • Autoimmunity*
  • Diabetes Mellitus / immunology
  • Gene Expression Regulation*
  • Glutamate Decarboxylase / genetics*
  • Glutamate Decarboxylase / immunology*
  • Glutamate Decarboxylase / physiology
  • Humans
  • Stiff-Person Syndrome / immunology
  • T-Lymphocytes / enzymology
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • Autoantibodies
  • gamma-Aminobutyric Acid
  • Glutamate Decarboxylase