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[参与1型糖尿病β细胞自身免疫性破坏的免疫机制]

[Immunologic mechanisms implicated in autoimmune destruction of beta cells in type I diabetes].

作者信息

Thivolet C

机构信息

Clinique Endocrinologique, Hôpital de l'Antiquaille, Lyon.

出版信息

Ann Endocrinol (Paris). 1992;53(3):78-81.

PMID:1295435
Abstract

Lymphocytic infiltration of the islets of Langerhans results from activation of immunity effector cells during the period preceding clinical onset of diabetes. After escape from thymic selection, the autoreactive cell clones proliferate in the peripheral hemopoietic organs prior to invading the islets of Langerhans. The selection, expansion and activation of autoreactive cells are under genetic control. The development of quantitative tests of cellular immunity should allow determination of the importance of the anti-islet immunologic reaction, suspected at present from the presence of specific autoantibodies in genetically predisposed subjects at high risk of insulin dependence.

摘要

朗格汉斯胰岛的淋巴细胞浸润是在糖尿病临床发作前的一段时间内免疫效应细胞激活所致。在逃脱胸腺选择后,自身反应性细胞克隆在外周造血器官中增殖,然后侵入朗格汉斯胰岛。自身反应性细胞的选择、扩增和激活受基因控制。细胞免疫定量检测方法的发展应有助于确定抗胰岛免疫反应的重要性,目前从有胰岛素依赖高风险的遗传易感性个体中存在特异性自身抗体推测存在这种反应。

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