Article
Altered expression of galectin-3 induces cortical thymocyte depletion and premature exit of immature thymocytes during Trypanosoma cruzi infection
Registro en:
MONTEIRO, Elizangela Silva et al. Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection. The American Journal of Pathology, v. 170, n. 2, p. 546-556, Feb. 2007.
0002-9440
10.2353/ajpath.2007.060389
Autor
Monteiro, Elizangela Silva
Lorenzato, Luciana Reis
Kenji Nihei, Oscar
Junqueira, Mara
Rabinovich, Gabriel Adrián
Hsu, Daniel Kaiyuan
Liu, Fu-Tong
Savino, Wilson
Chammas, Roger
Villa-Verde, Déa Maria Serra
Resumen
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. 2022-01-01