α-半乳糖神经酰胺在不同时间激活实验性自身免疫性重症肌无力小鼠NKT细胞对重症肌无力影响的研究

Research on the influence of α-GalCer activating experimental autoimmune myasthenia gravis mice NKT cells at different times on myasthenia gravis.

作者信息

Wang Y H, Jia J C, Liu G, Wang Y F

机构信息

Emergency Clinical Department, the First Affiliated Hospital, Henan Science and Technology University, Luoyang, China.

Molecular Biology Laboratory, the First Affiliated Hospital, Henan Science and Technology University, Luoyang, China.

出版信息

J Biol Regul Homeost Agents. 2015 Jan-Mar;29(1):195-200.

PMID:25864758

Abstract

This study aims to observe the effect of natural killer T (NKT) cell activation on experimental autoimmune myasthenia gravis (EAMG) model by injecting mice with α-GalCer in enterocoelia at different times, thus to provide a new therapy for EAMG. EAMG animal model of C57BL/6 mice was established and the mice were injected with α-GalCer irritant in enterocoelia. Vα14 NKT NKT cells were then activated through the transfer of CD1d. This paper discusses the effect of NKT cell activation on EAMG at different times by observing the variation of weight, clinical performance and relevant immunity indexes of mice. In C57BL/6 mice, the EAMG incidence rate of the Vehicle Group was 90%, the average onset duration was 37 ± 6 days; The incidence rate of α-GalCer prevention group was 30%;, the average onset duration was 51 ± 9 days. The forward immunization of α-GalCer activates NKT and protects C57BL/6 mice from the occurrence of EAMG, which provides basis for prevention and treatment of EAMG and other autoimmune diseases.

摘要

本研究旨在通过在不同时间经腹腔注射α-GalCer观察自然杀伤T（NKT）细胞激活对实验性自身免疫性重症肌无力（EAMG）模型的影响，从而为EAMG提供新的治疗方法。建立C57BL/6小鼠EAMG动物模型，并经腹腔给小鼠注射α-GalCer刺激剂。然后通过CD1d转移激活Vα14 NKT细胞。本文通过观察小鼠体重、临床表现及相关免疫指标的变化，探讨不同时间NKT细胞激活对EAMG的影响。在C57BL/6小鼠中，载体组EAMG发病率为90%，平均发病持续时间为37±6天；α-GalCer预防组发病率为30%，平均发病持续时间为51±9天。α-GalCer的提前免疫激活NKT并保护C57BL/6小鼠不发生EAMG，为EAMG及其他自身免疫性疾病的防治提供了依据。