Table 1.

Cytokines involved in the progression of atherosclerosis.

Involved stage	Component	Characteristics	Mechanisms in atherosclerosis	References
Recruitment	CCL2	Small proteins with four completely conserved cysteine residues, expressed by a variety of cell types	Guide Ly6Chigh monocytes to migrate into the subendothelial space and promote the bone marrow release of Ly6Chigh monocytes to the blood circulation	[15–17, 25–27]
	CCL5	Proteins secreted by monocyte, macrophages, T cells, and smooth muscle cells	Play a critical role in Ly6Clow monocytes' adhesion and recruitment	[13, 30, 33, 34]
	CXC3L1	Expressed by endothelial cells as a membrane-bound protein	Allow firm adhesion of monocytes on endothelial and smooth muscle cells independently of integrin activation and improve their survival from the bone marrow	[13, 14, 30–32]
Egress from the plaque	CCL19	Produced by stromal cells within primary and secondary lymphoid organs	Promote chemotactic migration of the macrophage to egress from the plaque	[38–41]
	CCL21	Produced by stromal cells within primary and secondary lymphoid organs and lymphatic endothelial cells (LECs) in peripheral tissues	Promote chemotactic migration of macrophage to egress from the plaque	[38–43]
Migration inhibition	Netrin-1	Neuronal guidance molecules expressed in many cells such as endothelial cells and foam cells	Inhibit the migration of monocytes into the intima and egress of macrophage from the plaque	[5, 9, 14, 47, 49, 51, 52]
	Semaphorin-3A	Secreted proteins expressed by endothelial cells and immune cells like macrophages	Act as a barrier to prevent monocyte adhesion and migration into the arterial intima during the early stage of atherogenesis	[57–60]
	Semaphorin-3E	Secreted, highly conserved, and matrix-associated proteins by macrophages, especially M1 macrophages	Inhibit macrophages migration and egress of macrophage from the plaque	[61, 62]