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半乳糖凝集素-9:动脉粥样硬化的抑制剂?

Galectin-9: A Suppressor of Atherosclerosis?

机构信息

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Immunol. 2020 Nov 4;11:604265. doi: 10.3389/fimmu.2020.604265. eCollection 2020.

DOI:10.3389/fimmu.2020.604265
PMID:33250901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7672040/
Abstract

It is no longer controversial that atherosclerosis is a vascular wall chronic inflammatory disease mediated by cells of innate and adaptive immunity. Galectin-9 (Gal-9) seems to be a crucial regulator of T-cell immunity by inducing apoptosis in specific T-cell subpopulations associated with autoimmunity and inflammatory disease. Accumulating evidence showed that galectin-9 signaling T-cell immunoglobulin mucin 3 (TIM-3) is concerned with different regulatory functions in autoimmunity, including direct depletion of pro-inflammatory T-cells, expanding the number of regulatory T cells, altering macrophages to an anti-inflammatory state and the induction of repressive myeloid-derived suppressor cells. In addition, anti-Tim-3-Ab administration increased atherosclerotic plaque formation by blocking Tim-3-galectin-9 interaction. Hence, we hypothesize that galectin-9 may be a novel therapy for atherosclerotic disease. Further researches are needed to investigate the precise effect of galectin-9 in the process of atherosclerosis.

摘要

人们已经不再争论动脉粥样硬化是一种由先天和适应性免疫细胞介导的血管壁慢性炎症性疾病。半乳糖凝集素-9(Gal-9)似乎通过诱导与自身免疫和炎症性疾病相关的特定 T 细胞亚群凋亡,成为 T 细胞免疫的关键调节剂。越来越多的证据表明,半乳糖凝集素-9信号转导 T 细胞免疫球蛋白粘蛋白 3(TIM-3)在自身免疫中涉及不同的调节功能,包括直接耗尽促炎 T 细胞、扩增调节性 T 细胞、将巨噬细胞改变为抗炎状态以及诱导抑制性髓源性抑制细胞。此外,抗 TIM-3-Ab 的给药通过阻断 TIM-3-半乳糖凝集素-9 相互作用增加了动脉粥样硬化斑块的形成。因此,我们假设半乳糖凝集素-9可能是动脉粥样硬化疾病的一种新的治疗方法。需要进一步研究以探讨半乳糖凝集素-9在动脉粥样硬化过程中的确切作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347d/7672040/eaafae015a1f/fimmu-11-604265-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347d/7672040/66b22d6b70c1/fimmu-11-604265-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347d/7672040/eaafae015a1f/fimmu-11-604265-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347d/7672040/66b22d6b70c1/fimmu-11-604265-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347d/7672040/eaafae015a1f/fimmu-11-604265-g002.jpg

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TIM‑3 inhibits PDGF‑BB‑induced atherogenic responses in human artery vascular smooth muscle cells.TIM-3 抑制人动脉血管平滑肌细胞中 PDGF-BB 诱导的动脉粥样硬化反应。
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T cell subsets and functions in atherosclerosis.
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Macrophage polarization markers in subcutaneous, pericardial, and epicardial adipose tissue are altered in patients with coronary heart disease.冠心病患者皮下、心包和心外膜脂肪组织中的巨噬细胞极化标志物发生改变。
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