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The "Leukocyte migration into central nervous system pathway" refers to a complex biological process by which immune cells—including lymphocytes and neutrophils—cross specialized barriers such as the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) to enter the central nervous system (CNS). This process is tightly regulated under normal conditions but is dramatically upregulated during neuroinflammatory diseases like multiple sclerosis, stroke, and Alzheimer’s disease. Key steps involve rolling, adhesion, arrest, and transmigration of leukocytes through endothelial cells lining CNS vessels. These steps are mediated by interactions between selectins, integrins (such as VLA‑4/α4β1), their ligands on endothelium (VCAM‑1/ICAM‑1), chemokines like CXCL12/CXCL10, and other adhesion molecules including CLMP. Therapeutic strategies targeting these molecular interactions—such as monoclonal antibodies against α4 integrin—have shown efficacy in reducing pathological immune cell infiltration but carry risks related to impaired host defense within the CNS[2][3][4][5]. Note: This entry describes a **pathway**, not a discrete molecular target or receptor. Therefore it does not fit standard conventions for therapeutic targets; instead it encompasses many interacting proteins that could individually be considered drug targets.
Mechanisms include inhibition of integrins or adhesion molecules to block leukocyte entry into the CNS; for example, natalizumab blocks α4 integrin/VLA‑4 to prevent immune cell transmigration.
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