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自发性糖尿病BB大鼠:导致自身免疫和糖尿病的缺陷部位。综述。

The spontaneously diabetic BB rat: sites of the defects leading to autoimmunity and diabetes mellitus. A review.

作者信息

Scott J

机构信息

Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908.

出版信息

Curr Top Microbiol Immunol. 1990;156:1-14. doi: 10.1007/978-3-642-75239-1_1.

Abstract

In summary, our bone marrow chimeras studies suggest that there are two defects in the BB rat associated with diabetes and/or lymphopenia, one residing at the level of the bone marrow lymphoid stem cell and the other within the T-cell differentiative environment, apparently postthymic. Our neonatal thymus transplantation studies and the adult thymus transplantation studies of others suggest a third defect in the BB rat, within the thymus itself, but this defect appears not to be responsible for the development of either the diabetes or the T lymphocytopenia. Rather, the thymic defect appears to control, at least in part, the lymphocyte hyporesponsiveness characteristic of the diabetes-prone BB rat. The role of the RT6 T-cell differentiation antigen in the etiopathogenesis of diabetes in this animal model remains unclear.

摘要

总之,我们的骨髓嵌合体研究表明,BB大鼠存在与糖尿病和/或淋巴细胞减少相关的两种缺陷,一种存在于骨髓淋巴干细胞水平,另一种存在于T细胞分化环境中,显然是在胸腺后。我们的新生胸腺移植研究以及其他人的成年胸腺移植研究表明,BB大鼠在胸腺本身存在第三种缺陷,但这种缺陷似乎与糖尿病或T淋巴细胞减少的发生无关。相反,胸腺缺陷似乎至少部分地控制了易患糖尿病的BB大鼠所特有的淋巴细胞低反应性。RT6 T细胞分化抗原在该动物模型糖尿病发病机制中的作用仍不清楚。

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