Data/hora: 01/06/2024 09:44:35

Provedor de dados: | 56
País: | Brazil
Título: | Cytokine production profile of heart-infiltrating T cells in Chagas' disease cardiomyopathy
Autores: | Cunha-Neto,E.; Rizzo,L.V.; Albuquerque,F.; Abel,L.; Guilherme,L.; Bocchi,E.; Bacal,F.; Carrara,D.; Ianni,B.; Mady,C.; Kalil,J.
Data: | 1998-01-01
Ano: | 1998
Palavras-chave: | Trypanosoma cruzi; Chagas' disease cardiomyopathy; Immunology; Cytokines; Gamma-interferon.
Resumo: | The hallmark of chronic Chagas' disease cardiomyopathy (CCC) is the finding of a T cell-rich inflammatory mononuclear cell infiltrate in the presence of extremely few parasites in the heart lesions. The scarcity of parasites in affected heart tissue casts doubt on the direct participation of Trypanosoma cruzi in CCC heart tissue lesions, and suggests the possible involvement of autoimmunity. The cells in the infiltrate are presumably the ultimate effectors of tissue damage, and there is evidence that such cells recognize cardiac myosin in molecular mimicry with T. cruzi proteins rather than primary reactivity to T. cruzi antigens (Cunha-Neto et al. (1996) Journal of Clinical Investigation, 98: 1709-1712). Recently, we have studied heart-infiltrating T cells at the functional level. In this short review we summarize the studies about the role of cytokines in human and experimental T. cruzi infection, along with our data on heart-infiltrating T cells in human Chagas' cardiomyopathy. The bulk of evidence points to a significant production of IFN-&lt;FONT FACE="Symbol"&gt;g&lt;/font&gt; and TNF-&lt;FONT FACE="Symbol"&gt;a&lt;/font&gt; which may be linked to T. cruzi-induced IL-12 production
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100018
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X1998000100018
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.31 n.1 1998
Fonte: | info:eu-repo/semantics/openAccess