Insulin-dependent diabetes mellitus and its animal models.
Major questions are still unanswered in the understanding of the pathogenesis of type 1 diabetes, including the important question of the nature of the autoantigen(s) recognised in the development of disease. In the nonobese diabetic mouse model, there is new evidence that insulin plays an important role: not only is it an antigen for pathogenic CD4+ T cells but also it is recognised by highly diabetogenic CD8+ T cells. Further studies using transgenic mice have also highlighted the role of glutamic acid decarboxylase as an autoantigen. It remains to be seen whether one or both of these autoantigens can be used in strategies to prevent human diabetes.
Wong
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FS
Section of Immunobiology, Yale School of Medicine, New Haven, CT 06520-8011, USA.
Janeway
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CA
D000818:Animals; D001324:Autoantigens / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D004195:Disease Models, Animal; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D008565:Membrane Proteins / Q000276:immunology; D051379:Mice; D016688:Mice, Inbred NOD; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000276:immunology; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8
D001324:Autoantigens; D008565:Membrane Proteins; C516862:PTPRN protein, human; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; C516863:Ptprn protein, mouse; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase