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Monocyte chemoattractant protein 2 (MCP-2, CCL8) and monocyte chemoattractant protein 3 (MCP-3, CCL7) are small, secreted cytokines belonging to the CC chemokine family. They play central roles in the immune system by attracting monocytes, lymphocytes, and other immune cells to sites of tissue injury, infection, or inflammation. MCP-2 and MCP-3 are produced by a variety of cell types in response to pro-inflammatory signals and act primarily through G protein-coupled receptors (notably CCR2, but also CCR1 and CCR3 for MCP-3). MCP-3 has the broadest activity spectrum among MCPs, activating monocytes, dendritic cells, lymphocytes, natural killer cells, eosinophils, basophils, and neutrophils, while MCP-2 also activates monocytes, lymphocytes, eosinophils, and basophils[1][2][3]. Both chemokines are implicated in the pathogenesis of inflammatory, autoimmune, and cardiovascular diseases as well as cancer, and are considered potential therapeutic targets for diseases characterized by pathological immune cell infiltration[1][3][4]. Blocking MCP-2 or MCP-3 activity, particularly via their receptors (such as CCR2), is under active investigation as a strategy for modulating immune responses in chronic inflammatory and autoimmune conditions[3][4].
Inhibition of chemokine–chemokine receptor interaction (blocking MCP-2 or MCP-3 binding to CCR2, CCR1, CCR3 prevents monocyte mobilization and leukocyte recruitment)
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