Cardiac myosin autoimmunity in acute Chagas' heart disease
Cardiac myosin autoimmunity in acute Chagas' heart disease
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DOI：
10.1128/iai.69.9.5643-5649.2001
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发表时间：
2001-09-01
影响因子：
3.1
通讯作者：
Engman, DM
中科院分区：
文献类型：
--
作者：
Leon, JS;Godsel, LM;Engman, DM
克氏锥虫（锥虫病的病原体）感染可能会诱导抗体和与自身抗原反应的T细胞（自身免疫）。由于自身免疫通常被认为是在感染的慢性阶段发展，一种假设是，自身免疫只有在自身反应细胞的长期低水平刺激后才会发展。然而，初步报告表明，自身免疫可能开始在急性T。克氏感染本研究的目的是探讨是否可以观察到心脏自身免疫性在急性T。克氏感染A/J小鼠感染巴西株T. cruzi在21天内患上了严重的心肌炎，并伴有体液和细胞自身免疫。具体来说，T。Cruzi感染诱导免疫球蛋白G（IgG）自身抗体和对心肌肌球蛋白的迟发型超敏反应（DTH）。这种自身免疫性类似于在用完全弗氏佐剂中的肌球蛋白免疫的A/J小鼠中发展的，其中肌球蛋白特异性抗体和DTH应答都在感染后或免疫后21天发展。T. Cruzi感染小鼠的DTH值略低于肌球蛋白免疫小鼠，但两组的肌球蛋白DTH值在统计学上相当。相反，C57 BL/6小鼠对肌球蛋白诱导的心肌炎及其相关的自身免疫具有抗性，其肌球蛋白IgG水平检测不到或较低，并且在T.克氏感染因此，体液和细胞心脏自身免疫可在急性T。遗传易感宿主中的克鲁兹感染。
Infection with Trypanosoma cruzi, the agent of Chagas' disease, may induce antibodies and T cells reactive with self antigens (autoimmunity). Because autoimmunity is generally thought to develop during the chronic phase of infection, one hypothesis is that autoimmunity develops only after long-term, low-level stimulation of self-reactive cells. However, preliminary reports suggest that autoimmunity may begin during acute T. cruzi infection. The goal of the present study was to investigate whether cardiac autoimmunity could be observed during acute T. cruzi infection. A/J mice infected with the Brazil strain of T. cruzi for 21 days developed severe myocarditis, accompanied by humoral and cellular autoimmunity. Specifically, T. cruzi infection induced immunoglobulin G (IgG) autoantibodies and delayed type hypersensitivity (DTH) to cardiac myosin. This autoimmunity resembles that which develops in A/J mice immunized with myosin in complete Freund's adjuvant in that myosin-specific antibodies and DTH responses both develop by 21 days postinfection or postimmunization. While the levels of myosin IgG in T. cruzi-infected mice were slightly lower than those in myosin-immunized mice, the magnitude of myosin DTH in the two groups was statistically equivalent. In contrast, C57BL/6 mice, which are resistant to myosin-induced myocarditis and its associated autoimmunity, developed undetectable or low levels of myosin IgG and did not exhibit myosin DTH or myocarditis upon T. cruzi infection. Therefore, humoral and cellular cardiac autoimmunity can develop during acute T. cruzi infection in the genetically susceptible host.