The regulation of inflammation by galectin-3

被引:440
作者
Henderson, Neil C. [1 ]
Sethi, Tariq [1 ]
机构
[1] Univ Edinburgh, Queens Med Res Inst, Ctr Inflammat Res, Edinburgh EH16 4TJ, Midlothian, Scotland
基金
英国惠康基金;
关键词
galectin-3; inflammation; neutrophil; macrophage; fibrosis; myofibroblast; ALTERNATIVE MACROPHAGE ACTIVATION; TUMOR-ASSOCIATED MACROPHAGES; HEPATIC STELLATE CELLS; HUMAN LUNG FIBROBLASTS; IGE-BINDING PROTEIN; AIRWAY INFLAMMATION; MURINE MACROPHAGES; ADHESION MOLECULE; HUMAN NEUTROPHILS; DENDRITIC CELLS;
D O I
10.1111/j.1600-065X.2009.00794.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Galectin-3 is a beta-galactoside-binding animal lectin of appro- ximately 30 kDa and is evolutionarily highly conserved. Galectin-3 is promiscuous, its localization within the tissue micro-environment may be extracellular, cytoplasmic, or nuclear, and it has a concentration-dependent ability to be monomeric or form oligomers. These properties impart great flexibility on galectin-3 as a specific regulator of many biological systems including inflammation. For example, in acute tissue damage galectin-3 is a key component in the host defense against microbes such as Streptococcus pneumoniae. However, if tissue injury becomes repetitive galectin-3 also appears to be intimately involved in the transition to chronic inflammation, facilitating the walling off of tissue injury with fibrogenesis and organ scarring. Therefore galectin-3 can be viewed as a regulatory molecule acting at various stages along the continuum from acute inflammation to chronic inflammation and tissue fibrogenesis. In this review, we examine the role of galectin-3 in inflammation, and discuss the manipulation of galectin-3 expression as a potentially novel therapeutic strategy in the treatment of a broad range of inflammatory diseases.
引用
收藏
页码:160 / 171
页数:12
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