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C-C motif chemokine ligand 7 (CCL7), formerly known as monocyte chemoattractant protein 3 (MCP-3), is a versatile chemokine that plays a pivotal role in the recruitment and activation of various leukocytes, including monocytes, eosinophils, and T lymphocytes [8, 12]. It is produced by a wide range of cells, such as macrophages and fibroblasts, and exerts its biological effects by binding to several G protein-coupled receptors, most notably CCR1, CCR2, CCR3, and CCR5 [11, 19]. This multi-receptor interaction makes CCL7 a critical orchestrator of the inflammatory response and immune surveillance [13, 14]. In the context of disease, CCL7 is implicated in chronic inflammatory conditions and the progression of multiple cancers, where it facilitates tumor cell invasion, migration, and the establishment of a pro-tumorigenic microenvironment [1, 21]. Additionally, elevated serum levels of CCL7 have been explored as biomarkers for disease risk and therapeutic efficacy in conditions like schizophrenia and certain solid tumors [5, 22]. Therapeutic interventions targeting the CCL7 pathway generally involve receptor antagonists, particularly those targeting CCR2 and CCR5, to block pathological cell trafficking and suppress excessive inflammation or tumor growth [8, 16].
Inhibition of the CCL7 signaling axis through antagonism of cognate CC chemokine receptors, primarily CCR2 and CCR5, to block leukocyte recruitment and inflammatory signal transduction; Neutralization of the CCL7 ligand using specific monoclonal antibodies or experimental chemokine-binding proteins like evasins to prevent receptor activation [8, 13, 14].
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