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病毒诱导的糖尿病。没有证据表明脑心肌炎病毒D变种破坏β细胞存在免疫机制。

Virus-induced diabetes mellitus. No evidence for immune mechanisms in the destruction of beta-cells by the D-variant of encephalomyocarditis virus.

作者信息

Yoon J W, McClintock P R, Bachurski C J, Longstreth J D, Notkins A L

出版信息

Diabetes. 1985 Sep;34(9):922-5. doi: 10.2337/diab.34.9.922.

Abstract

A possible contribution of the immune system to the pathogenesis of virus-induced diabetes mellitus was investigated using the D-variant of encephalomyocarditis (EMC-D) virus. Studies on the F1 and backcross progeny of susceptible and resistant strains of mice gave no suggestion of a linkage between susceptibility and the major histocompatibility locus. Immuno-suppression by antilymphocyte serum did not prevent the induction of EMC-D-induced diabetes. Athymic nude mice infected with EMC-D virus showed a nearly identical diabetogenic response as compared with heterozygous littermates. Passive transfer of lymphocytes from mice made diabetic with EMC-D virus into normal mice failed to produce diabetes. From these and other studies, we conclude that the development of EMC-D-induced diabetes is due to the direct destruction of beta-cells by the virus and that the contribution of the immune response to the pathogenesis of this disease is, at the most, minor.

摘要

利用脑心肌炎(EMC-D)病毒的D变种,研究了免疫系统在病毒诱导的糖尿病发病机制中的可能作用。对易感和抗性小鼠品系的F1及回交后代的研究未发现易感性与主要组织相容性位点之间存在连锁关系。抗淋巴细胞血清诱导的免疫抑制并不能阻止EMC-D诱导的糖尿病的发生。感染EMC-D病毒的无胸腺裸鼠与杂合子同窝小鼠相比,表现出几乎相同的致糖尿病反应。将感染EMC-D病毒而患糖尿病的小鼠的淋巴细胞被动转移到正常小鼠中未能引发糖尿病。从这些研究及其他研究中,我们得出结论,EMC-D诱导的糖尿病的发生是由于病毒对β细胞的直接破坏,并且免疫反应对该疾病发病机制的作用至多是次要的。

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