• activation/memory markers;
  • Chagas disease;
  • chronic myositis;
  • DAF knock-out;
  • pathogenesis


Introduction: Murine infection with Trypanosoma cruzi (Tc) has been used to study the role of T-cells in the pathogenesis of human inflammatory idiopathic myositis. Absence of decay-accelerating factor 1 (Daf1) has been shown to enhance murine T-cell responses and autoimmunity. Methods: To determine whether Daf1 deficiency can exacerbate Tc-induced myositis, C57BL/6 DAF+/+ and DAF−/− mice were inoculated with 5 × 104 trypomastigotes, and their morbidity, parasitemia, parasite burden, histopathology, and T-cell expansion were studied in the acute and chronic stages. Results: DAF−/− mice had lower parasitemia and parasite burden but higher morbidity, muscle histopathology, and increased number of CD44+ (activated/memory phenotype) splenic CD4+ and CD8+ T-cells. Conclusions: An enhanced CD8+ T-cell immune-specific response may explain the lower parasitemia and parasite burden levels and the increase in histopathological lesions. We propose that Tc-inoculated DAF−/− mice are a useful model to study T-cell mediated immunity in skeletal muscle tissues. Muscle Nerve 46: 582–587, 2012