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 via 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.
Highlights
Discovered as a potent eosinophil chemoattractant [1], Galectin-9 (Gal-9) is recently regarded as a multifaceted immune regulator that affects a host of cell types
We found that of oxidized low-density lipoprotein inhibited atherosclerosis process via decreasing Th17 cell number [18]
Gal-9, the ligand of T-cell immunoglobulin mucin 3 (Tim-3), affects the function of several immune cells such as monocytes, effector T cells, and macrophages, especially regulatory T cells, which are proven involved in atherosclerosis
Summary
Discovered as a potent eosinophil chemoattractant [1], Galectin-9 (Gal-9) is recently regarded as a multifaceted immune regulator that affects a host of cell types. Studies have shown that activated Treg cells inhibit the process of atherosclerotic disease, and Forkhead box protein P3 (FOXP3) expression controls the transcription program that plays a protective role in atherosclerotic plaques [19].
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