Acosta A M, Santos-Buch C A
Circulation. 1985 Jun;71(6):1255-61. doi: 10.1161/01.cir.71.6.1255.
Antiheart immune reactions have been reported in patients with Chagas' disease, and we have postulated that the observed cardiac lesions are mediated by autoimmune antiheart reactions elicited by the etiologic agent Trypanosoma cruzi. In this report, BALB/c mice infected with a low inoculum of T. cruzi developed splenic lymphocyte cytotoxicity against normal syngeneic neonatal cardiac myofibers in vitro 150 days after infection, whereas splenic lymphocytes obtained from mice at 15, 45, 90, or 120 days after infection or from matched controls did not. No antiheart antibody or antibody-directed cellular cytotoxicity was observed, nor was there an increase in natural killer cell activity. Hearts from mice studied at 150 days after infection showed mononuclear cell myocarditis with myocytolysis in the absence of intracellular T. cruzi forms. Hearts from the other mice did not exhibit any histologic changes. Other reports from our laboratory have identified a cross-reacting antigen (SRA) shared by T. cruzi and striated muscle. Immunization of BALB/c mice with SRA produced immunopathogenic dynamics similar to those seen with long-term T. cruzi infection. Collectively these data indicate that the cardiac lesions seen in patients with Chagas' disease may be attributed to autoimmune reactions elicited by cross-reacting antigens of T. cruzi and striated muscle.
恰加斯病患者中已报告存在抗心脏免疫反应，我们推测观察到的心脏病变是由病原体克氏锥虫引发的自身免疫性抗心脏反应介导的。在本报告中，感染低剂量克氏锥虫的BALB/c小鼠在感染150天后，其脾淋巴细胞在体外对正常同基因新生心肌纤维产生了细胞毒性，而在感染后15、45、90或120天从小鼠或匹配对照中获得的脾淋巴细胞则没有。未观察到抗心脏抗体或抗体介导的细胞毒性，自然杀伤细胞活性也没有增加。感染150天后研究的小鼠心脏显示单核细胞性心肌炎伴肌细胞溶解，且不存在细胞内克氏锥虫形态。其他小鼠的心脏未表现出任何组织学变化。我们实验室的其他报告已鉴定出克氏锥虫和横纹肌共有的一种交叉反应抗原（SRA）。用SRA免疫BALB/c小鼠产生的免疫致病动态与长期克氏锥虫感染所见相似。这些数据共同表明，恰加斯病患者所见的心脏病变可能归因于克氏锥虫和横纹肌交叉反应抗原引发的自身免疫反应。
