半乳糖凝集素
炎症
免疫系统
半乳糖凝集素-1
促炎细胞因子
细胞生物学
生物
背景(考古学)
聚糖
凝集素
分泌物
内质网
调节器
高尔基体
免疫学
生物化学
糖蛋白
基因
古生物学
作者
Anabela M. Cutine,Camila A Bach,Florencia Veigas,Joaquín Pedro Merlo,Lorena Laporte,Montana N Manselle Cocco,Mora Massaro,Nicolás Sarbia,Ramiro Martin Perrotta,Yamil D Mahmoud,Gabriel A. Rabinovich
出处
期刊:Glycobiology
[Oxford University Press]
日期:2021-01-22
卷期号:31 (8): 891-907
被引量:13
标识
DOI:10.1093/glycob/cwab007
摘要
The relevance of glycan-binding proteins in immune tolerance and inflammation has been well established, mainly by studies of C-type lectins, siglecs and galectins, both in experimental models and patient samples. Galectins, a family of evolutionarily conserved lectins, are characterized by sequence homology in the carbohydrate-recognition domain, atypical secretion via an endoplasmic reticulum-Golgi-independent pathway and by the ability to recognize β-galactoside-containing saccharides. Galectin-1 (Gal-1), a prototype member of this family, displays mainly anti-inflammatory and immunosuppressive activities, although, similar to many cytokines and growth factors, it may also trigger paradoxical pro-inflammatory effects under certain circumstances. These dual effects could be associated to tissue-, time- or context-dependent regulation of galectin expression and function, including particular pathophysiologic settings and/or environmental conditions influencing the structure of this lectin, as well as the availability of glycosylated ligands in immune cells during the course of inflammatory responses. Here, we discuss the tissue-specific role of Gal-1 as a master regulator of inflammatory responses across different pathophysiologic settings, highlighting its potential role as a therapeutic target. Further studies designed at analyzing the intrinsic and extrinsic pathways that control Gal-1 expression and function in different tissue microenvironments may contribute to delineate tailored therapeutic strategies aimed at positively or negatively modulating this glycan-binding protein in pathologic inflammatory conditions.
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