在T细胞介导的自身免疫中,分子模拟:病毒激活了针对髓基蛋白特异的人类T细胞克隆
K W Wucherpfennig1, J L Strominger
1Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138.
病毒和髓基蛋白 (MBP) 之间的分子模拟可以触发自身免疫反应. T细胞受体可以从不同的病原体中识别结构相似的,从而促进自身免疫.
科学领域:
- 免疫学 免疫学 免疫学
- 这是一种自身免疫力.
- 分子仿真是分子仿真.
背景情况:
- 病毒T细胞表位和自我之间的结构相似性可以触发自身免疫反应.
- 髓基蛋白 (MBP) 是多发性硬化症 (MS) 的关键自身抗原.
研究的目的:
- 为了研究病毒和MBP之间的分子模仿.
- 识别模仿MBP并激活T细胞的病毒或细菌.
主要方法:
- 开发了基于MBP的MHCII类结合和TCR识别的数据库搜索标准.
- 选了129种,以检测它们激活MS患者的MBP特异性T细胞克隆的能力.
主要成果:
- 七个病毒和一个细菌激活了MBP特异性的T细胞克隆.
- 只有一个可以通过序列对齐来识别为分子模拟物.
- 一个单一的T细胞受体识别了不同的,但结构相关的.
结论:
- 结构模仿,而不是序列身份,对于T细胞通过交叉反应表位素激活至关重要.
- 这种交叉反应性对了解像MS这样的自身免疫性疾病的病原发生有重大影响.
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