Cunha-Neto E, Rizzo L V, Albuquerque F, Abel L, Guilherme L, Bocchi E, Bacal F, Carrara D, Ianni B, Mady C, Kalil J
Laboratório de Imunologia de Transplantes, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, Brasil.
Braz J Med Biol Res. 1998 Jan;31(1):133-7. doi: 10.1590/s0100-879x1998000100018.
The hallmark of chronic Chagas' disease cardiomyopathy (CCC) is the finding of a T cell-rich inflammatory mononuclear cell infiltrate in the presence of extremely few parasites in the heart lesions. The scarcity of parasites in affected heart tissue casts doubt on the direct participation of Trypanosoma cruzi in CCC heart tissue lesions, and suggests the possible involvement of autoimmunity. The cells in the infiltrate are presumably the ultimate effectors of tissue damage, and there is evidence that such cells recognize cardiac myosin in molecular mimicry with T. cruzi proteins rather than primary reactivity to T. cruzi antigens (Cunha-Neto et al. (1996) Journal of Clinical Investigation, 98: 1709-1712). Recently, we have studied heart-infiltrating T cells at the functional level. In this short review we summarize the studies about the role of cytokines in human and experimental T. cruzi infection, along with our data on heart-infiltrating T cells in human Chagas' cardiomyopathy. The bulk of evidence points to a significant production of IFN-gamma and TNF-alpha which may be linked to T. cruzi-induced IL-12 production.
慢性恰加斯病性心肌病（CCC）的标志是在心脏病变中存在极少量寄生虫的情况下，发现富含T细胞的炎性单核细胞浸润。在受影响的心脏组织中寄生虫数量稀少，这使人怀疑克氏锥虫是否直接参与了CCC心脏组织病变，并提示自身免疫可能发挥了作用。浸润的细胞大概是组织损伤的最终效应细胞，有证据表明这些细胞通过与克氏锥虫蛋白的分子模拟识别心肌肌球蛋白，而非对克氏锥虫抗原的主要反应性（库尼亚 - 内托等人，《临床研究杂志》，1996年，98卷：1709 - 1712页）。最近，我们在功能水平上研究了浸润心脏的T细胞。在这篇简短的综述中，我们总结了关于细胞因子在人类和实验性克氏锥虫感染中的作用的研究，以及我们关于人类恰加斯病性心肌病中浸润心脏的T细胞的数据。大量证据表明会大量产生干扰素 - γ和肿瘤坏死因子 - α，这可能与克氏锥虫诱导的白细胞介素 - 12产生有关。
