Abstract
The pathogenesis of chronic chagasic cardiomyophathy 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 cardiomyophathy.