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(American Journal of Pathology. 2007;170:546-556.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060389

Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection

Elizangela Silva-Monteiro*, Luciana Reis Lorenzato*, Oscar Kenji Nihei*, Mara Junqueira{dagger}{ddagger}, Gabriel Adrián Rabinovich§, Daniel Kaiyuan Hsu, Fu-Tong Liu, Wilson Savino*, Roger Chammas{dagger} and Déa Maria Serra Villa-Verde*

From the Department of Pathology{ddagger} and the Laboratory of Thymus Research, Department of Immunology,* Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; the Laboratory of Experimental Oncology,{dagger} Faculty of Medicine, University of São Paulo, São Paulo, Brazil; the Division of Immunogenetics,§ Hospital de Clínicas "José de San Martín," Faculty of Medicine, University of Buenos Aires, Buenos Aires, Argentina; and the Department of Dermatology, University of California, Los Angeles, California

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 the endogenous lectin galectin-3 in accelerating death of thymocytes and migration of these cells away from the thymus after T. cruzi infection. We observed a pronounced increase in galectin-3 expression that paralleled the extensive depletion of CD4+CD8+ immature thymocytes after infection. In vitro, recombinant galectin-3 induced increased levels of death in cortical immature thymocytes. Consistent with the role of galectin-3 in promoting cell death, thymuses from gal-3–/– mice did not show cortical thymocyte depletion after parasite infection in vivo. In addition, galectin-3 accelerated laminin-driven CD4+CD8+ thymocyte migration in vitro and in vivo induced exportation of CD4+CD8+ cells from the thymus to the peripheral compartment. Our findings provide evidence of a novel role for galectin-3 in the regulation of thymus physiology and identify a potential mechanism based on protein-glycan interactions in thymic atrophy associated with acute T. cruzi infection.




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