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鉴定实验性自身免疫性心内膜炎中链球菌 M 蛋白的心脏毒性表位。

Identification of streptococcal m-protein cardiopathogenic epitopes in experimental autoimmune valvulitis.

机构信息

Department of Biological Sciences, California State University, Sacramento, CA, USA.

出版信息

J Cardiovasc Transl Res. 2014 Mar;7(2):172-81. doi: 10.1007/s12265-013-9526-4. Epub 2013 Dec 18.

Abstract

The M protein of rheumatogenic group A streptococci induces carditis and valvulitis in Lewis rats and may play a role in pathogenesis of rheumatic heart disease. To identify the epitopes of M5 protein that produce valvulitis, synthetic peptides spanning A, B, and C repeat regions contained within the extracellular domain of the streptococcal M5 protein were investigated. A repeat region peptides NT4, NT5/6, and NT7 induced valvulitis similar to the intact pepsin fragment of M5 protein. T cell lines from rats with valvulitis recognized M5 peptides NT5/6 and NT6. Passive transfer of an NT5/6-specific T cell line into naïve rats produced valvulitis characterized by infiltration of CD4+ cells and upregulation of VCAM-1, while an NT6-specific T cell line did not target the valve. Our new data suggests that M protein-specific T cells may be important mediators of valvulitis in the Lewis rat model of rheumatic carditis.

摘要

致风湿性 A 组链球菌的 M 蛋白可诱导刘易斯大鼠的心膜炎和瓣膜病,并且可能在风湿性心脏病的发病机制中起作用。为了鉴定产生心膜炎的 M5 蛋白表位,研究了包含在链球菌 M5 蛋白细胞外结构域内的 A、B 和 C 重复区的合成肽。重复区肽 NT4、NT5/6 和 NT7 诱导的瓣膜病类似于 M5 蛋白的完整胃蛋白酶片段。来自有心膜炎的大鼠的 T 细胞系识别 M5 肽 NT5/6 和 NT6。将 NT5/6 特异性 T 细胞系被动转移到幼稚大鼠中会产生以 CD4+细胞浸润和 VCAM-1 上调为特征的心膜炎,而 NT6 特异性 T 细胞系则不会靶向瓣膜。我们的新数据表明,M 蛋白特异性 T 细胞可能是风湿性心脏病的刘易斯大鼠模型中心膜炎的重要介导者。

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