<原著>NODマウスにおけるインスリン自己抗体と抗glutamic acid decarboxylase抗体の検討

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Evidence indicates that insulin-dependent diabetes mellitus (IDDM) is an autoimmune disorder which is associated with the development of autoantibodies including insulin autoantibodies (IAA), islet cell autoantibodies (ICA) and autoantibodies against 64kD islet protein. Of these autoantibodies, those against the 64kD islet protein are being increasingly accepted as directing to glutamic acid decarboxylase (GAD) in the pancreatic β cells. In the present study, IAA and anti-GAD antibodies were measured in the NOD mouse, which is a well-established animal model of IDDM, in order to investigate the pathological significance of both antibodies in IDDM. Anti-GAD antibodies as well as IAA were evaluated using enzyme-linked immunosorbent assays developed in this laboratory. In the observation of NOD mice, anti-GAD antibodies were detected at 4 weeks of age, while IAA were not found until the age of 12 weeks. The levels of both IAA and anti-GAD antibodies were significantly higher in diabetic NOD mice than in non-diabetic NOD mice. However, there was no correlation between the titers of IAA and anti-GAD antibodies. In non-diabetic NOD mice, both IAA and anti-GAD antibody levels broadly increased with age. By contrast, control ICR mice did not show any age-related increase in titers of IAA or anti-GAD antibodies. In view of the fact that cyclophosphamide (CY) promotes the onset of diabetes in NOD mice, IAA and anti-GAD antibodies were measured in CY-treated NOD mice. In NOD females, IAA levels were not changed following CY treatment during the observation period of 3 weeks, while anti-GAD antibodies significantly increased at 2 weeks after CY treatment. Thus, anti-GAD antibodies seem to arise earlier in the development of IDDM than IAA.
近畿大学の論文
1993-03-25

著者

飯尾一也
近畿大学医学部第2内科学教室

<原著>NODマウスにおけるインスリン自己抗体と抗glutamic acid decarboxylase抗体の検討

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