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CD99 molecule-like 2 (CD99L2) is a type I transmembrane glycoprotein expressed on both vascular endothelial cells and leukocytes[1][3][4]. It is critically involved in controlling the process of leukocyte extravasation during inflammation by facilitating the diapedesis of neutrophils and monocytes across the endothelial barrier. CD99L2 functions as a homophilic cell adhesion molecule at endothelial junctions and regulates a unique step in leukocyte transendothelial migration, operating between the action of PECAM-1 (CD31) and CD99. Inhibition or knockout of CD99L2 impairs leukocyte recruitment to inflamed tissues, highlighting its central role in immune cell trafficking during inflammation[1][4]. Its modulation is a potential therapeutic strategy for regulating inflammatory responses, though no approved drugs currently target CD99L2 directly.
Antibody blockade impairs leukocyte transmigration by preventing homophilic adhesion at the endothelial barrier[1][4]
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