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Mem. Inst. Oswaldo Cruz ; 100(supl.1): 93-96, Mar. 2005.
Article in English | LILACS | ID: lil-402181

ABSTRACT

The comprehension of the pathogenesis of Trypanosoma cruzi-elicited myocarditis is crucial to delineate new therapeutic strategies aiming to ameliorate the inflammation that leads to heart dysfunction, without hampering parasite control. The augmented expression of CCL5/RANTES and CCL3/MIP-1alpha, and their receptor CCR5, in the heart of T. cruzi-infected mice suggests a role for CC-chemokines and their receptors in the pathogenesis of T. cruzi-elicited myocarditis. Herein, we discuss our recent results using a CC-chemokine receptor inhibitor (Met-RANTES), showing the participation of CC-chemokines in T. cruzi infection and unraveling CC-chemokine receptors as an attractive therapeutic target for further evaluation in Chagas disease.


Subject(s)
Animals , Mice , Chagas Cardiomyopathy/drug therapy , /analogs & derivatives , Chemokines, CC/metabolism , Myocarditis/drug therapy , Receptors, Chemokine/antagonists & inhibitors , Trypanosoma cruzi , /immunology , /immunology , Chagas Cardiomyopathy/immunology , Chagas Cardiomyopathy/metabolism , /therapeutic use , Chemotaxis, Leukocyte/immunology , Myocarditis/immunology , Myocarditis/metabolism , Myocarditis/parasitology , Trypanosoma cruzi/immunology
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