Galectin-3 regulates expression of extracellular matrix molecules and receptors in Trypanosoma cruzi-infected mice

E SILVA-MONTEIRO, L.R. BERBERT, R. CHAMMAS, G.A. RABINOVICH, W. SAVINO, D.M.S. VILLA-VERDE

Córdoba, Argentina

Congreso; VII Congress of the Latin American Society of Immunology; 2005

Latin American Society of Immunology

During acute infection with Trypanosoma cruzi, the causative agent of Chagas´ disease, the thymus undergoes intense atrophy followed by a premature escape of CD4+CD8+ immature cortical thymocytes. Here we report a pivotal role for galectin-3, an endogenous lectin found at sites of T-cell maturation and activation, in accelerating thymocyte death and migration following T. cruzi infection. A pronounced increase in galectin-3 expression paralleled the extensive depletion of CD4+CD8+ immature thymocytes following infection with this protozoan parasite. In vitro, exposure to recombinant galectin-3 resulted in increased levels of apoptosis of cortical immature thymocytes. Consistently thymuses from gal-3-/- mice did not show cortical thymocyte depletion following parasite infection in vivo. In addition, galectin-3 accelerated laminin-driven CD4+CD8+ thymocyte migration, suggesting another potential mechanism of export of CD4+CD8+ cells from the thymus to the peripheral compartment. Our findings provide evidence of a novel role of galectin-3 in the regulation of thymus physiology and identify potential mechanisms based on protein-glycan interactions to understand thymic atrophy associated with acute T. cruzi infection.