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Immune cell recruitment is a fundamental biological process involving the migration of leukocytes from the systemic circulation into peripheral tissues to facilitate host defense and tissue repair [4, 14, 16]. This orchestrated event proceeds through a multi-step cascade—rolling, activation, firm adhesion, and diapedesis—mediated by interactions between cell adhesion molecules, such as selectins and integrins, and chemokines with their corresponding G protein-coupled receptors [3, 4, 16]. While essential for health, dysregulated recruitment is a primary driver of pathology in autoimmune disorders, chronic inflammatory diseases, and the tumor microenvironment, where it can promote immunosuppression or tissue destruction [3, 4, 14]. Therapeutic strategies frequently target specific nodes in this process, such as blocking alpha-4 integrins or antagonizing receptors like CCR5 or CXCR4, to prevent the influx of pathogenic cells into tissues like the gut or central nervous system [4, 11]. Because it involves a diverse network of distinct molecular families rather than a single protein, it is characterized as a physiological process rather than a discrete molecular therapeutic target [4, 9].
Therapeutic agents modulate the recruitment process by inhibiting cell adhesion molecules (e.g., integrin alpha-4), antagonizing chemokine receptors (e.g., CCR5, CXCR4, CCR4), or neutralizing chemoattractant ligands to prevent the pathological infiltration of leukocytes into specific tissue compartments [4, 11, 17].
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