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日本脑炎病毒感染中低血糖的诱导:T淋巴细胞的作用

Induction of hypoglycaemia in Japanese encephalitis virus infection: the role of T lymphocytes.

作者信息

Khanna N, Mathur A, Bharadwaj M, Chaturvedi U C

机构信息

Postgraduate Department of Microbiology, K.G. Medical College, Lucknow, India.

出版信息

Clin Exp Immunol. 1997 Feb;107(2):282-7. doi: 10.1111/j.1365-2249.1997.281-ce1173.x.

Abstract

We report here development of hypoglycaemia in the convalescent phase of Japanese encephalitis virus (JEV) infection in mice by the induction of antigen-specific Ly1- 2+ T cells in the spleen which mediate hypoglycaemia through the generation of soluble T cell hypoglycaemic factor (TCHF). The TCHF acted in a dose-dependent manner and was found to be trypsin-sensitive and thermolabile. It was purified on Superose-12 high performance liquid chromatography (HPLC) gel filtration column and purified protein migrated as a approximately 25-kD band on SDS-PAGE. The JEV-induced hypoglycaemia coincided with an increased circulating glucagon level, without any alterations in blood insulin and growth hormone concentrations. These effects were mimicked by TCHF. These results indicate that JEV-primed T lymphocytes mediate hypoglycaemia through the production of a soluble hypoglycaemic factor.

摘要

我们在此报告,小鼠感染日本脑炎病毒(JEV)恢复期出现低血糖,这是由脾脏中抗原特异性Ly1-2⁺ T细胞的诱导所致,这些T细胞通过产生可溶性T细胞低血糖因子(TCHF)介导低血糖。TCHF呈剂量依赖性作用,且对胰蛋白酶敏感、热不稳定。它在Superose-12高效液相色谱(HPLC)凝胶过滤柱上纯化,纯化后的蛋白质在SDS-PAGE上迁移为约25-kD条带。JEV诱导的低血糖与循环中胰高血糖素水平升高同时出现,而血液胰岛素和生长激素浓度无任何变化。TCHF模拟了这些效应。这些结果表明,JEV激活的T淋巴细胞通过产生可溶性低血糖因子介导低血糖。

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