Table 1.

Summary of data of CCR5 and its ligands, primary source, main effects, and main references.

Gene name	Expressed by/primary source	Main effects		References
		Pro-inflammation	Endothelium repair and angiogenesis
CCL3	Monocytes/macrophages, T cells, vascular smooth muscle cells, eosinophils, coronary endothelial cells, and platelets.	Mediates the recruitment of macrophages into the injured site by binding with its receptor, CCR5.	CCL3 induces the infiltration of macrophages into the damaged retina and produces vascular endothelial growth factor (VEGF) by binding to CCR5, and eventually promotes corneal neovascularization.	Ridiandries et al., 2016; Menten et al., 2002; DiPietro et al., 1998; Lu et al., 2008.
CCL4	Monocyte, T cells, B lymphocytes, NK cells, dendritic cells, vascular smooth muscle cells, and neutrophils.	Chemoattractants for immature dendritic cells and macrophages/monocytes, attracts macrophages to destroy islet cells.	Increases VEGF-C expression and promotes lymph angiogenesis in oral cancer cells.	Ridiandries et al., 2016; Menten et al., 2002; Chang and Chen, 2016; Lien et al., 2018.
CCL5	T-cells, epithelial cells and activated platelets	Mediates the macrophage recruitment and M1/M2 phenotype switching, recruits leukocytes and certain natural-killer cells, promotes smooth muscle cells phenotypic switching from the contractile to synthetic phenotype.	CCL5 is pro-angiogenic in the ischemic tissues and subcutaneous model, promotes the revascularization and muscle regeneration by binding to its receptor, CCR5.	Suffee et al., 2012; Liu et al., 2014; Zhang et al., 2015b; Ridiandries et al., 2016; Lin et al., 2018.
CCR5	Monocytes/macrophages, activated T cells, endothelial cells, endothelial progenitor cells (EPCs), natural killer cells, astrocytes, microglia, and neurons.	Promotes infiltration of monocytes/macrophages to the injured site, aggravates hepatic steatosis and insulin resistance, and increases triglyceride synthesis.	Accelerates the homing of EPCs to damaged endothelial cells, promoting endothelial repair or the formation of neovascularization.	Suffee et al., 2017; Bjerregaard et al., 2019; Rookmaaker et al., 2007; Potteaux et al., 2006; Berres et al., 2010; Ishida et al., 2012; Kitade et al., 2012; Shen et al., 2013; Liu et al., 2014; Zhang et al., 2015b; Ridiandries et al., 2016; Perez-Martinez et al., 2018; Yan et al., 2019.