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Muscle Nerve ; 46(4): 582-7, 2012 Oct.
Article in English | MEDLINE | ID: mdl-22987701

ABSTRACT

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 × 10(4) 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.


Subject(s)
CD55 Antigens/genetics , Chagas Disease/immunology , Myositis/immunology , Myositis/parasitology , Trypanosoma cruzi/immunology , Animals , CD55 Antigens/metabolism , Chagas Disease/genetics , Chagas Disease/parasitology , Chronic Disease , Disease Models, Animal , Humans , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Myositis/genetics , T-Lymphocytes/immunology , T-Lymphocytes/metabolism , T-Lymphocytes/pathology , Trypanosoma cruzi/growth & development
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