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Tissue-specific control of galectin-1-driven circuits during inflammatory responses

期刊

GLYCOBIOLOGY
卷 31, 期 8, 页码 891-907

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/glycob/cwab007

关键词

autoimmunity; cancer; chronic inflammation; galectin-1; glycoimmunology

资金

  1. Agencia Nacional de Promocion Cientifica y Tecnologica [PICT 2014-3687, 2017-0494]
  2. Fundacion Sales
  3. Fundacion Bunge Born
  4. Fundacion Baron
  5. Richard Lounsbery Foundation

向作者/读者索取更多资源

The importance of glycan-binding proteins, especially galectins, in immune tolerance and inflammation has been well established. Galectin-1, as a prototype member of this protein family, displays mainly anti-inflammatory and immunosuppressive activities but may also have pro-inflammatory effects under certain circumstances. Further studies on the regulation and function of galectins in different tissue microenvironments could lead to tailored therapeutic strategies for pathological inflammatory conditions.
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 beta-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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