title: Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of Schistosoma mansoni infection.
abstract: 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.
authors.affiliation: Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. felipe@histo.ufrj.br
authors.forename: Felipe L
authors.initials: FL
authors.lastname: Oliveira
authors.forename: Camila
authors.initials: C
authors.lastname: Brand
authors.forename: Adelzon A
authors.initials: AA
authors.lastname: Paula
authors.forename: Kátia D
authors.initials: KD
authors.lastname: Arcanjo
authors.forename: Daniel K
authors.initials: DK
authors.lastname: Hsu
authors.forename: Fu-Tong
authors.initials: FT
authors.lastname: Liu
authors.forename: Christina M
authors.initials: CM
authors.lastname: Takiya
authors.forename: Radovan
authors.initials: R
authors.lastname: Borojevic
authors.forename: Roger
authors.initials: R
authors.lastname: Chammas
authors.forename: Márcia C
authors.initials: MC
authors.lastname: El-Cheikh
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D001402:B-Lymphocytes / Q000166:cytology* / Q000378:metabolism*; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D037502:Galectin 3 / Q000235:genetics / Q000378:metabolism*; D007150:Immunohistochemistry; D008198:Lymph Nodes / Q000166:cytology*; D008297:Male; D051379:Mice; D010587:Phagocytosis / Q000235:genetics / Q000502:physiology; D010950:Plasma Cells / Q000166:cytology / Q000378:metabolism; D012550:Schistosoma mansoni / Q000472:pathogenicity*; D012555:Schistosomiasis mansoni / Q000235:genetics / Q000378:metabolism*
chemical_list: D037502:Galectin 3