The involvement of laminin in anti-myocardial cell autoimmune response in murine Chagas disease.
The pathogenesis of chronic chagasic cardiomyopathy associated with Chagas disease is still controversial, although evidence indicates a T cell-dependent autoimmune process. Using a mouse model for chronic Chagas disease, we previously evidenced that hearts grafted within the ears of Trypanosoma cruzi infected syngeneic recipients were rejected through a CD4+ T cell-dependent mechanism. Moreover, we showed that such a process was dependent on laminin-mediated interactions, since it could be abrogated by anti-laminin or anti-laminin receptor antibodies. In this review the same passive cell transfer model is considered for discussion: the participation of the laminin alteration in the composition of the inflammatory infiltrate formed in response to the antimyocardial autoreactive CD4+ T cells, as well as the presence of laminin-binding cytokines. Finally we suggest the existence of a relationship between the inflammatory infiltrate, the laminin contents and deposition of pro-inflammatory laminin-binding cytokines, which may act in concert during the generation of Chagas disease-related cardiomyopathy.
Silva-Barbosa
S D
SD
Department of Immunology and Institute Oswaldo Cruz, Foundation Oswaldo Cruz, Rio de Janeiro, Brazil. suse@gene.dbbm.fiocruz.br
Savino
W
W
D000818:Animals; D015551:Autoimmunity; D002598:Chagas Cardiomyopathy / Q000276:immunology*; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D007797:Laminin / Q000032:analysis / Q000502:physiology*; D051379:Mice; D009206:Myocardium / Q000276:immunology*; D013601:T-Lymphocytes / Q000502:physiology
D016207:Cytokines; D007797:Laminin