Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
PLoS One. 2011 May 6;6(5):e19216. doi: 10.1371/journal.pone.0019216.
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.
半乳糖凝集素-3 是一种 β-半乳糖苷结合蛋白，已被证明可调节包括细胞激活、分化和凋亡在内的病理生理过程。最近，我们发现半乳糖凝集素-3 可作为 B 细胞分化为浆细胞的有效抑制剂。在此，我们使用野生型（WT）和半乳糖凝集素-3（-/-）小鼠，研究了半乳糖凝集素-3 是否会干扰慢性日本血吸虫病期间肠系膜淋巴结（MLN）中 B 细胞区室的淋巴组织。日本血吸虫合成 GalNAcβ1-4（Fucα1-3）GlcNAc（Lac-DiNAc）结构（N-乙酰半乳糖胺β1-4-N-乙酰葡萄糖胺），已知这些结构与半乳糖凝集素-3 相互作用并引发强烈的体液反应。来自卵和成虫的抗原不断引流至 MLN，并诱导多克隆 B 细胞激活。在本研究中，我们观察到慢性感染的半乳糖凝集素-3（-/-）小鼠的巨噬细胞和 B 淋巴细胞数量显著减少，随后 MLN 中的 B 淋巴细胞和浆细胞龛发生剧烈的组织学变化。缺乏半乳糖凝集素-3 有利于增加淋巴滤泡数量，但使滤泡细胞更容易受到凋亡刺激。在血吸虫病过程中，有过多的凋亡小体、更高数量的 Annexin V（+）/PI（-）细胞，并且滤泡细胞的清除减少。在此，我们观察到半乳糖凝集素-3 在非淋巴滤泡细胞中表达，其缺失与组织结构的严重损伤有关。因此，我们提供了关于半乳糖凝集素-3 在调节与 B 淋巴细胞和浆细胞龛、凋亡、吞噬和细胞周期特性相关的组织学事件中的作用的新信息，在感染日本血吸虫的小鼠 MLN 中。
