MCP-1, CCL2 is a member of the CC ß chemokine family. It is widely expressed in endothelial cells, smooth muscle cells and monocytes in response to several atherogenic stimulants such as CD40 ligand, platelet derived growth factor (PDGF), interleukin-1beta (IL-1beta) and oxidized low density lipoprotein. Several recent in vivo studies have disclosed critical roles of MCP1 in atherosclerosis. In addition, MCP-1 has been implicated in monocytic infiltration of tissues during several inflammatory diseases, and has been implicated in macrophage-mediated tumor growth suppression in mice. CCL2 has been shown to have direct effects on tumor cells in an autocrine and paracrine fashion in multiple cancers, including breast, lung, cervix, ovary, sarcoma, and prostate. In addition, MCP-1 plays a key role in the regulation of MMPs during transmigration. Ccl2 induces migration of MonoMac6 by induction of MMP2. MCP-1 and Ccl3/MIP-1alpha mediate firm adherence and (subsequent) transmigration of neutrophils via protein synthesis and secondary generation of leukotrienes and PAF, which in turn directly activate neutrophils in mouse cremaster muscle. MCP-1 is induced from endothelial cells by MIF and from fetal skin fibroblast by IL-17.