心力衰竭合并cvb3感染病毒性心肌炎大鼠抗原特异性的自反应T细胞表达分析

Expression analysis of antigen-specific self-reactive T cells in heart failure rats infected with vire myocarditis with cvb3

目的 探究心力衰竭合并cvb3感染病毒性心肌炎大鼠抗原特异性的自反应T细胞表达特征。方法 研究对象选取A/J雄性大鼠合计30只,建立慢性心力衰竭模型后随机分为对照组及感染组,感染组使用CVB3菌株感染,比较两组大鼠心脏和胰腺病理学变化;获取大鼠淋巴细胞,使用IA k/IE k右旋聚体对细胞染色后进行流式细胞术检测,观察大鼠Myhc 334-352、ANT 21-40、BCKDk 111-130、SERCA2a 971-990和β1 AR 181-200/211-230特异性抗原T细胞表达。结果 感染组大鼠胰腺及心脏组织表现出心房炎症浸润,心肌浸润伴坏死和矿化,胰腺炎症浸润、萎缩和坏死/矿化,呈现炎症损伤;感染组淋巴结淋巴细胞Myhc 334-352、SERCA2a 971-990抗原特异性的自反应T细胞表达高于对照组(P<0.05),两组ANT 21-40、BCKDk 111-130、β1 AR 181-200/211-230抗原特异性的自反应T细胞表达差异无统计学意义(P>0.05);感染组肝脏淋巴细胞Myhc 334-352、SERCA2a 971-990、ANT 21-40抗原特异性的自反应T细胞表达高于对照组(P<0.05),两组BCKDk 111-130、β1 AR 181-200/211-230抗原特异性的自反应T细胞表达差异无统计学意义(P>0.05);感染组心脏淋巴细胞Myhc 334-352、SERCA2a 971-990抗原特异性的自反应T细胞表达高于对照组(P<0.05),两组ANT 21-40、BCKDk 111-130、β1 AR 181-200/211-230抗原特异性的自反应T细胞表达差异无统计学意义(P>0.05)。结论 心力衰竭合并cvb3感染病毒性心肌炎大鼠表现出心脏及胰腺炎性损伤,CVB3感染可能导致具有多种抗原特异性的致病性自身反应性T细胞的产生,其中以Myhc 334-352、SERCA2a 971-990为主,T细胞可能是CVB3感染中心脏自身免疫的主要介质。

Objective To investigate the expression characteristics of antigen-specific self-reactive T cells in rats with heart failure combined with cvb3 infection with viral myocarditis.Methods A total of 30 male A/J rats were selected to establish a chronic heart failure model and randomly divided into control group and infection group.The infection group was infected with CVB3 strain,and the pathological changes of the heart and pancreas of the two groups were compared.Rat lymphocytes were obtained,stained with IA k/IE k right-handed polymers and detected by flow cytometry.The expression of Myhc 334-352,ANT 21-40,BCKDk 111-130,SERCA2a 971-990 andβ1AR181-200/211-230 specific antigen T cells were observed.Results In the infected group,the pancreas and heart tissues showed atrial inflammatory infiltration,myocardial infiltration with necrosis and mineralization,and pancreatic inflammatory infiltration,atrophy and necrosis/mineralization with inflammatory injury.The expression of antigen-specific T cells Myhc 334-352 and SERCA2a 971-990 in lymph node lymphocytes of infection group was higher than that of control group(P<0.05).There was no significant difference in the expression of antigen-specific ANT 21-40,BCKDk 111-130,β1AR 181-200/211-230 T cells between the two groups(P>0.05).The expression of antigen-specific T cells Myhc 334-352,SERCA2a 971-990 and ANT 21-40 in liver lymphocytes of infection group was higher than that of control group(P<0.05).There was no significant difference in the expression of antig-specific self-reactive T cells of BCKDk 111-130 and p1AR 181-200/211-230 between the two groups(P>0.05).The expression of antigen-specific T cells Myhc 334-352 and SERCA2a 971-990 in cardiac lymphocytes in the infected group was higher than that in the control group(P<0.05).There was no significant difference in the expression of antigen-specific ANT 21-40,BCKDk 111-130,β1AR 181-200/211-230 T cells between the two groups(P>0.05).Conclusion Rats with heart failure combined with cvb3 infection with viral myocarditis show inflammatory damage to the heart and pancreas,and CVB3 infection may lead to the production of a variety of antigenspecific pathogenic autoreactive T cells,mainly Myhc 334-352 and SERCA2a 971-990.T cells may be the main mediator of cardiac autoimmunity in CVB3 infection.