Departments of Pathology and Microbiology-Immunology, Northwestern University, Feinberg Cardiovascular Research Institute, Chicago, IL, USA.
Parasite Immunol. 2013 Jan;35(1):1-10. doi: 10.1111/pim.12008.
Cardiac inflammation that develops during infection with Trypanosoma cruzi may result in part from autoimmunity, which may occur after bystander activation, after parasite-induced cardiomyocyte damage, or molecular mimicry. A/J mice infected with T. cruzi or immunized with heat-killed T. cruzi (HKTC) develop strong autoimmunity accompanied by cardiac damage. To determine whether this cardiac damage occurs via an antibody-dependent mechanism, we analysed T. cruzi-infected and HKTC-immunized mice for the presence of autoantibodies, cardiac antibody deposition, and serum cardiac troponin I as a measure of cardiac damage. We also performed a serum transfer experiment in which sera from T. cruzi-infected and T. cruzi-immunized mice (and controls) were transferred into naïve recipients, which were then analysed for the presence of antibodies and serum troponin. Unlike T. cruzi-infected mice, T. cruzi-immunized mice did not show significant antibody deposition in the myocardium. These results indicate that antibody deposition does not precede cardiac damage and inflammation in mice immunized with or infected with T. cruzi. Serum adoptive transfer did not induce cardiac damage in any recipients. Based on these findings, we conclude that the cardiac damage induced by immunization with HKTC is not mediated by antibodies.
在感染克氏锥虫期间发生的心脏炎症可能部分是由于自身免疫引起的，这可能发生在旁观者激活后、寄生虫诱导的心肌细胞损伤后或分子模拟后。感染克氏锥虫或用热灭活的克氏锥虫（HKTC）免疫的 A/J 小鼠会产生强烈的自身免疫反应，并伴有心脏损伤。为了确定这种心脏损伤是否通过抗体依赖性机制发生，我们分析了感染克氏锥虫和 HKTC 免疫的小鼠是否存在自身抗体、心脏抗体沉积以及血清心肌肌钙蛋白 I 作为心脏损伤的指标。我们还进行了血清转移实验，将来自感染克氏锥虫和克氏锥虫免疫的小鼠（和对照）的血清转移到未感染的受体中，然后分析抗体和血清肌钙蛋白的存在情况。与感染克氏锥虫的小鼠不同，克氏锥虫免疫的小鼠心肌中没有明显的抗体沉积。这些结果表明，抗体沉积并不先于感染或免疫克氏锥虫的小鼠的心脏损伤和炎症。血清过继转移未在任何受者中引起心脏损伤。基于这些发现，我们得出结论，用 HKTC 免疫引起的心脏损伤不是由抗体介导的。
