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Selectin L, commonly known as CD62L, is a type I transmembrane cell adhesion molecule and a member of the selectin family. It is constitutively expressed on most circulating leukocytes, including naive and central memory T cells, where it mediates the initial 'rolling' step of the leukocyte adhesion cascade by binding to carbohydrate ligands on the vascular endothelium (1.1.1, 1.3.1). This process is essential for the homing of lymphocytes to secondary lymphoid organs via high endothelial venules (HEVs) and for the recruitment of immune cells to sites of inflammation (1.3.1, 1.4.4). In clinical practice, CD62L serves as a critical biomarker for T cell differentiation, distinguishing central memory T cells (CD62L-high) from effector memory T cells (CD62L-low), which has significant implications for the persistence and efficacy of CAR-T cell therapies (1.1.2, 1.4.1, 1.5.2). CD62L is also implicated in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) and non-alcoholic steatohepatitis (NASH), and it acts as an adhesion receptor for viruses like HIV-1 (1.2.2, 1.3.2, 1.3.5). Therapeutic strategies targeting CD62L include the use of pan-selectin inhibitors like bimosiamose to reduce excessive inflammation and the engineering of T cells to maintain CD62L expression for improved anti-tumor activity (1.2.1, 1.4.2, 1.5.2).
Inhibition of leukocyte-endothelial adhesion and rolling; blockade of lymphocyte homing to secondary lymphoid organs; prevention of viral entry; enhancement of CAR-T cell persistence through maintained expression.
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