Cunha-Neto E, Kalil J
Immunology Laboratory of Transplantation, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, Brazil.
Sao Paulo Med J. 1995 Mar-Apr;113(2):757-66. doi: 10.1590/s1516-31801995000200005.
The time scale dissociation between high parasitemia and tissue pathology, allied to the absence of parasites in the heart lesions of chronic Chagas' disease cardiopathy, casted doubt on the direct participation of Trypanosoma cruzi in tissue lesions. Moreover, the heart tissue lesions in chronic Chagas' disease cardiopathy are associated to an inflammatory mononuclear cell infiltrate, presumably the ultimate effectors of tissue damage. It has been hypothesized that the inflammatory cell infiltrate could mediate a delayed hypersensitivity process directed to the heart tissue components, an autoimmune response triggered by immunological cross-reactivity in the course of a protective immune response against some T. cruzi antigen homologous to heart proteins. However, little is known about the effector role of the T cells in the infiltrate, or about the nature of the antigen that lead to their accumulation in tissue. In this paper, we will review the published evidence on autoimmunity and immunological cross-reactivity between T. cruzi and the mammalian host, along with data generated in our laboratory. The definition of the precise role played by autoimmunity in the pathogenesis of Chagas' disease cardiopathy may have important consequences both for immunoprophylaxis and for the therapeutic approach of chronic Chagas' disease.
高寄生虫血症与组织病理学之间的时间尺度分离，再加上慢性恰加斯病心肌病心脏病变中不存在寄生虫，这让人怀疑克氏锥虫是否直接参与了组织病变。此外，慢性恰加斯病心肌病的心脏组织病变与炎症性单核细胞浸润有关，推测炎症性单核细胞浸润是组织损伤的最终效应因子。有人提出假设，炎症细胞浸润可能介导针对心脏组织成分的迟发型超敏反应过程，这是一种在针对某些与心脏蛋白同源的克氏锥虫抗原的保护性免疫反应过程中，由免疫交叉反应引发的自身免疫反应。然而，对于浸润中的T细胞的效应作用，或者导致它们在组织中积累的抗原的性质，人们了解甚少。在本文中，我们将回顾已发表的关于克氏锥虫与哺乳动物宿主之间自身免疫和免疫交叉反应的证据，以及我们实验室生成的数据。明确自身免疫在恰加斯病心肌病发病机制中所起的确切作用，可能对免疫预防和慢性恰加斯病的治疗方法都产生重要影响。
