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Decay‐accelerating factor 1 deficiency exacerbates Trypanosoma cruzi ‐induced murine chronic myositis
Author(s) -
Solana María E.,
Ferrer María F.,
Novoa María Mercedes,
Song WenChao,
GÓmez Ricardo M.
Publication year - 2012
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.23347
Subject(s) - parasitemia , myositis , immunology , biology , pathogenesis , cd8 , immune system , histopathology , trypanosoma cruzi , plasmodium berghei , t cell , autoimmunity , pathology , medicine , parasite hosting , plasmodium falciparum , malaria , anatomy , computer science , world wide web
: 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. Muscle Nerve 46: 582–587, 2012