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Developmental Immunology
Volume 7, Issue 2-4, Pages 293-301

The Involvement of Laminin in Anti-Myocardial Cell Autoimmune Response in Murine Chagas Disease

1Laboratory on Thymus Research, Department of Immunology, Institute Oswaldo Cruz, Foundation Oswaldo Cruz, Rio de Janeiro, Brazil
2Laboratory on Cell Markers, Center for Bone Marrow Transplantation, National Cancer Institute, Rio de Janeiro, Brazil
3Laboratory on Thymus Research, Department of Immunology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Ave. Brasilo 4365 Manguinhos, Rio de Janeiro 21045-000, Brazil

Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.