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公共实验技术中心免疫学技术平台举办SCI论文报告会(三)
2021-05-29 12:36:36  来源:   点击:

2021年5月14日,公共实验技术中心免疫学技术平台在科技大楼13-2室举办了SCI论文报告会,研究生梁嘉钰作了题目为“Th1 Biased Progressive Autoimmunity in AgedAire-Deficient MiceAccelerated Thymic Epithelial Cell Senescence”的报告。会议由公共实验技术中心免疫学技术平台主任袁青教授主持,平台师生16人参加了本次会议。

报告内容主要介绍了虽然自身免疫性疾病,如类风湿性关节炎和系统性红斑狼疮,经常与胸腺过早衰老有关,但自身免疫性疾病和胸腺萎缩之间缺乏直接联系。作者监测了缺陷小鼠胸腺退化的进程,在缺陷小鼠中,有缺陷的阴性选择会导致自身免疫的自发和渐进性发展。与年龄匹配的野生型小鼠相比,老年缺陷小鼠的胸腺细胞总数和新近迁出的胸腺细胞数量较少,而β-GAL+胸腺上皮细胞数量较多。这种现象可能部分归因于同源于胸腺的活化Th1细胞数量的增加。弗氏完全佐剂免疫反复挑战后,胸腺老化增强支持了这一推测。综上所述,本研究的重点是一种独特的机制,即自身免疫通过返回Th1细胞促进胸腺上皮细胞的衰老。

在会议中,参会师生就相关内容进行了交流和探讨。此次报告紧紧围绕免疫学技术平台目前开展的科研方向,展示了最新研究前沿和动态;开拓了师生科研思路,为后续课题设计、课题开展提供了指导,同时也锻炼了师生SCI论文的阅读、分析、写作能力,浓厚了免疫学技术平台的学术氛围。

Th1 Biased Progressive Autoimmunity in AgedAire-Deficient Mice Accelerated Thymic Epithelial Cell Senescence

ABSTRACT: Although autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus, are frequently associated with premature aging of the thymus, a direct link is missing between autoimmunity and thymic atrophy. Here we monitored the progression of thymic involution in Aire-deficient mice, in which defective negative selection causes spontaneous and progressive development of autoimmunity. In young and middle-aged mice, Aire deficiency appeared to be protective as supported by the reduced β-gal+ epithelial cells and the enhanced thymic output. However, once the autoimmune phenotype was fully developed in aged Airedeficient mice, their thymuses underwent accelerated involution. In comparison to the age-matched wildtype littermates, old Aire-deficient mice showed lower numbers of total thymocytes and recent thymic emigrants but more β-gal+ thymic epithelial cells. This phenomenon may partly be attributable to the increased number of activated Th1 cells homing to the thymus. This speculation was further supported by the enhanced thymic aging following repeated challenges with complete Freund’s adjuvant immunization. Taken together, the present study highlights a unique mechanism by which autoimmunity facilitates the senescence of thymic epithelial cells through returning Th1 cells.

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