The role of galectins in the regulation of autophagy and inflammasome in host immunity

被引:1
|
作者
Lo, Tzu-Han [1 ]
Weng, I-Chun [1 ]
Chen, Hung-Lin [2 ]
Liu, Fu-Tong [1 ,3 ]
机构
[1] Acad Sinica, Inst Biomed Sci, Taipei 11529, Taiwan
[2] Acad Sinica, Inst Biol Chem, Taipei 11529, Taiwan
[3] Univ Southern Calif, Dept Dermatol, Keck Sch Med, Los Angeles, CA 90033 USA
关键词
Galectins; Glycans; Infection; Autophagy; Inflammasome; GUANYLATE-BINDING-PROTEINS; NLRP3; INFLAMMASOME; GLYCAN INTERACTIONS; INNATE; CLEARANCE; RECEPTORS; PHOSPHORYLATION; ACTIVATION; PATHOGEN; AMPK;
D O I
10.1007/s00281-024-01018-5
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Galectins, a family of glycan-binding proteins have been shown to bind a wide range of glycans. In the cytoplasm, these glycans can be endogenous (or "self"), originating from damaged endocytic vesicles, or exogenous (or "non-self"), found on the surface of invading microbial pathogens. Galectins can detect these unusual cytosolic exposures to glycans and serve as critical regulators in orchestrating immune responses in innate and adaptive immunity. This review provides an overview of how galectins modulate host cellular responses, such as autophagy, xenophagy, and inflammasome-dependent cell death program, to infection.
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收藏
页数:13
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