Figure 2.

CX₃CL1 from endothelial cell affects CX₃CR1-expressing cells within blood vessels. For angiogenesis, monocytes expressing CX₃CR1 promoted by CX₃CL1 can secret cytokines and VEGF. This can lead to formation of extracellular matrix and vascular remodeling for angiogenesis. For inflammation, activation of CX₃CR1 which is expressed in PBMCs causes leukocytes to migrate to the site of inflammation. CX₃CR1-expressing Th1 also stimulates inflammation by secretion of IFN-γ and IL-12. For plaque, when CX₃CL1 binds to CX₃CR1 on monocyte, macrophage, and foam cells, these cells will accumulate in blood vessels and promote cell survival via expressing anti-apoptotic Bcl2 within cells. CX₃CR1 is required for atherosclerosis. For aplastic anemia, autoreactive T cells expressing CX₃CR1 are recruited into bone marrow by CX₃CL1 to destroy HPSCs, resulting in aplastic anemia.

VEGF, vascular endothelial growth factor; PBMC, peripheral blood mononuclear cell; HPSC, hematopoietic stem cell; EC, endothelial cell; HIF, hypoxia-inducible factor; MAPK, mitogen-activated protein kinase; GPA, granulomatosis with polyangiitis.