Lack of Galectin-3 Disturbs Mesenteric Lymph Node Homeostasis and B Cell Niches in the Course of Schistosoma mansoni Infection

PLoS One

Daniel K. Hsu¹  Fu-Tong Liu¹  Márcia C. El-Cheikh²  Roger Chammas³  Christina M. Takiya⁴  Felipe L. Oliveira⁵  Kátia D. Arcanjo⁵  Radovan Borojevic⁵  Adelzon A. Paula⁵  Camila Brand⁵ 

[1] Department of Dermatology, School of Medicine, University of California Davis, Sacramento, California, United States of America;Instituto do Câncer do Estado de São Paulo, São Paulo, Brazil;Laboratório de Oncologia Experimental, Departamento de Radiologia e Oncologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil;Laboratório de Patologia Celular – Instituto de Ciências Biomédicas – Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil;Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

关键词: B cells;    Apoptosis;    Plasma cells;    Macrophages;    Cell differentiation;    Schistosomiasis;    Cell cycle and cell division;    Lymph nodes;   

DOI  :  10.1371/journal.pone.0019216

学科分类：医学（综合）

来源: Public Library of Science

【 摘 要 】

Galectin-3 is a β-galactoside-binding protein that has been shown to regulate pathophysiological processes, including cellular activation, differentiation and apoptosis. Recently, we showed that galectin-3 acts as a potent inhibitor of B cell differentiation into plasma cells. Here, we have investigated whether galectin-3 interferes with the lymphoid organization of B cell compartments in mesenteric lymph nodes (MLNs) during chronic schistosomiasis, using WT and galectin-3-/- mice. Schistosoma mansoni synthesizes GalNAcβ1-4(Fucα1-3)GlcNAc(Lac-DiNAc) structures (N-acetylgalactosamine β1-4 N-acetylglucosamine), which are known to interact with galectin-3 and elicit an intense humoral response. Antigens derived from the eggs and adult worms are continuously drained to MLNs and induce a polyclonal B cell activation. In the present work, we observed that chronically-infected galectin-3-/- mice exhibited a significant reduced amount of macrophages and B lymphocytes followed by drastic histological changes in B lymphocyte and plasma cell niches in the MLNs. The lack of galectin-3 favored an increase in the lymphoid follicle number, but made follicular cells more susceptible to apoptotic stimuli. There were an excessive quantity of apoptotic bodies, higher number of annexin V+/PI- cells, and reduced clearance of follicular apoptotic cells in the course of schistosomiasis. Here, we observed that galectin-3 was expressed in non-lymphoid follicular cells and its absence was associated with severe damage to tissue architecture. Thus, we convey new information on the role of galectin-3 in regulation of histological events associated with B lymphocyte and plasma cell niches, apoptosis, phagocytosis and cell cycle properties in the MLNs of mice challenged with S.mansoni.

【 授权许可】

CC BY