诱导GAD65特异性调节性T细胞可抑制非肥胖糖尿病小鼠中持续的自身免疫性糖尿病。

Induction of GAD65-specific regulatory T-cells inhibits ongoing autoimmune diabetes in nonobese diabetic mice.

作者信息

Tisch R, Liblau R S, Yang X D, Liblau P, McDevitt H O

机构信息

Department of Microbiology and Immunology, Stanford University Medical Center, California, USA.

出版信息

Diabetes. 1998 Jun;47(6):894-9. doi: 10.2337/diabetes.47.6.894.

DOI:10.2337/diabetes.47.6.894

PMID:9604865

Abstract

IDDM is a T-cell-mediated autoimmune disease in which the insulin-producing beta-cells are destroyed. The disease process is complex, involving the recognition of several beta-cell autoantigens. One of these, GAD65, appears to have a critical and not fully defined role in IDDM in humans and in the NOD mouse. We provide evidence that an ongoing diabetogenic response in NOD mice can be suppressed after intravenous administration of GAD65, but not by other beta-cell autoantigens. Furthermore, suppression of the diabetogenic response is mediated by the induction of GAD65-specific CD4+ regulatory T-cells. Finally, cytokine analysis indicates that these CD4+ regulatory T-cells have a T-helper 2 phenotype.

摘要

胰岛素依赖型糖尿病（IDDM）是一种由T细胞介导的自身免疫性疾病，其中产生胰岛素的β细胞被破坏。疾病过程复杂，涉及多种β细胞自身抗原的识别。其中之一，谷氨酸脱羧酶65（GAD65），在人类和非肥胖糖尿病（NOD）小鼠的IDDM中似乎具有关键但尚未完全明确的作用。我们提供的证据表明，静脉注射GAD65后可抑制NOD小鼠中正在进行的致糖尿病反应，但其他β细胞自身抗原则不能。此外，致糖尿病反应的抑制是由GAD65特异性CD4 +调节性T细胞的诱导介导的。最后，细胞因子分析表明这些CD4 +调节性T细胞具有辅助性T细胞2型表型。