Decay-accelerating factor 1 deficiency exacerbates Trypanosoma cruzi-induced murine chronic myositis

SOLANA M; FERRER M; NOVOA M; SONG WC; RICARDO M GOMEZ

MUSCLE & NERVE

JOHN WILEY & SONS INC

Lugar: New York; Año: 2012

0148-639X

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 Tcinduced myositis, C57BL/6 DAFþ/þ 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 CD44þ (activated/memory phenotype) splenic CD4þ and CD8þ T-cells. Conclusions: An enhanced CD8þ 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.