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Trypanosoma Cruzi-Sensitized T-Lymphocyte Mediated ⁵¹Cr Release from Human Heart Cells in Chagas' Disease^*

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. These findings appear to indicate that T-lymphocytes from patients with Changas' 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.

Accepted for publication June 17, 1978.

^* This work was supported by grants 7113/75 and 2600/75 from the Conselho Nacional de Desenvolvimento Cientifico e Tecnológico do Brasil.

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