Teixeira A R, Teixeira G, Macêdo V, Prata A
Am J Trop Med Hyg. 1978 Nov;27(6):1097-1107. doi: 10.4269/ajtmh.1978.27.1097.
Cytotoxicity of T-lymphocytes from patients with Chagas' disease to parasitized and non-parasitized human heart cells labelled with 51Cr was demonstrated. The highest ratio of 51Cr released from the normal, non-parasitized heart cells was observed when the T-lymphocytes were collected from patients with acute Chagas' disease. The quantity of 51Cr released from the normal heart cells that were destroyed by T-lymphocytes collected from patients with chronic Chagas' disease was also significantly higher than the quantity of 51Cr released from normal heart cells incubated with lymphocytes from normal donors. The specific release of 51Cr from the heart cell cultures destroyed by the immune T-lymphocytes from patients with acute Chagas' disease and from patients with chronic disease was 38.1% and 25.8%, respectively, compared to the release of 51Cr observed in control studies. A small particle human heart cell antigen was shown to inhibit the migration of Trypanosoma cruzi-immune peripheral blood leukocytes. The findings appear to indicate that T-lymphocytes from patients with Chagas' disease are susceptible to activation by a cross-reactive heart cell antigen and suggest that an autoimmune mechanism can be established in some cases of acute Chagas' disease and can be perpetuated in the chronic phase of this disease by the continuous antigenic stimulation. Further, these experimental data indicate that the autoimmune destruction of heart cells in Chagas' disease is produced by delayed-type hypersensitivity mediated by T. cruzi-sensitized T-lymphocytes.
已证实恰加斯病患者的T淋巴细胞对用51Cr标记的被寄生虫感染和未被寄生虫感染的人心脏细胞具有细胞毒性。当从急性恰加斯病患者中收集T淋巴细胞时，观察到正常的、未被寄生虫感染的心脏细胞释放51Cr的比例最高。慢性恰加斯病患者的T淋巴细胞破坏正常心脏细胞后释放的51Cr量，也显著高于与正常供体淋巴细胞共同孵育的正常心脏细胞释放的51Cr量。与对照研究中观察到的51Cr释放量相比，急性恰加斯病患者和慢性恰加斯病患者的免疫T淋巴细胞破坏的心脏细胞培养物中51Cr的特异性释放率分别为38.1%和25.8%。一种小颗粒人心脏细胞抗原被证明可抑制克氏锥虫免疫外周血白细胞的迁移。这些发现似乎表明，恰加斯病患者的T淋巴细胞易被交叉反应性心脏细胞抗原激活，并提示在某些急性恰加斯病病例中可建立自身免疫机制，且在该疾病的慢性期可通过持续的抗原刺激而持续存在。此外，这些实验数据表明，恰加斯病中心脏细胞的自身免疫性破坏是由克氏锥虫致敏的T淋巴细胞介导的迟发型超敏反应产生的。
