TRANSGENIC MICE WITH I-A ON ISLET CELLS ARE NORMOGLYCEMIC BUT IMMUNOLOGICALLY INTOLERANT
TRANSGENIC MICE WITH I-A ON ISLET CELLS ARE NORMOGLYCEMIC BUT IMMUNOLOGICALLY INTOLERANT
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DOI：
10.1126/science.2499048
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发表时间：
1989-06-09
期刊：
影响因子：
56.9
通讯作者：
MATHIS, D
中科院分区：
文献类型：
--
作者：
BOHME, J;HASKINS, K;MATHIS, D
胰岛素依赖型糖尿病（IDDM）是由胰腺朗格汉斯岛分泌胰岛素的β细胞特异性丧失引起的。有人提出，这些细胞上主要组织相容性复合体（MHC） II类分子的异常表达可能是其自身免疫损害的触发因素。在胰岛细胞表面表达同种异体或同基因II类分子的转基因小鼠中对这一建议进行了测试，其表达水平与正常情况下在静止的B细胞上发现的水平相当。这些动物不会患糖尿病，也没有观察到胰岛的淋巴细胞浸润。这种免疫失活不是由于对“外来”II类分子的耐受。
Insulin-dependent diabetes mellitus (IDDM) is caused by a specific loss of the insulin-producing beta cells from pancreatic Langerhans islets. It has been proposed that aberrant expression of major histocomaptibility complex (MHC) class II molecules on these cells could be a triggering factor for their autoimmune destriction. This proposal was tested in transgenic mice that express allogeneic or syngeneic class II molecules on the surface of islet cells at a level comparable with that normally found on resting B lumphocytes. These animals do not develop diabetes, nor is lymphocyte infiltration of the islets observed. This immunological inactivity does not result from tolerance to the "foreign" class II molecules.