Regulation of leukocyte migration by activation of the leukocyte adhesion molecule-1 (LAM-1) selectin

Abstract

A central feature of host defence is the ability of leukocytes to enter tissues in response to immune or inflammatory stimuli. The leukocyte adhesion molecule-1 (LAM-1) regulates the migration of human leukocytes by mediating the binding both of lymphocytes to high endothelial venules of peripheral lymph nodes and of neutrophils to endothelium at inflammatory sites. As lymphocytes and neutrophils express the same LAM-1 protein, it is not clear how lineage-specific differences in leukocyte migration are controlled. We now report that the affinity of LAM-1 for a carbohydrate-based ligand, PPME, is dramatically increased following lymphocyte and neutrophil activation by lineage-specific stimuli. In addition, activation of lymphocytes by physiological stimuli enhanced LAM-1-dependent binding to high endothelial venules. Thus, transient changes in LAM-1 affinity after leukocyte stimulation probably directly influence leukocyte migration.

Ubc9 Is Required for Positive Selection and Late-Stage Maturation of Thymocytes

“…Reduced cell numbers of mature SP cells in the thymus from Ubc9 fl/fl Cd4Cre mice might be attributed to dysregulation of thymocytes migration, decreased cell survival, or defect in the acquisition of proliferation competence during maturation. CCR7 and CD62L expression are required for cortex-medulla intrathymic migration or thymic emigration, respectively (31,32). However, both CCR7 and CD62L expression on CD4 SP cells were intact in the absence of Ubc9 (Supplemental Fig.…”

Functional features of neutrophils induced by G-CSF and GM-CSF treatment: differential effects and clinical implications

“…73 Kinetic studafter short exposure of neutrophils to G-CSF. 146 LAM-1 has been shown to play an essential role in leukocyte rolling along ies could demonstrate maximal levels of expression 8-12 h after a single administration of G-CSF. 70, 71 Concentration of endothelium, the first step of the adhesion cascade.…”

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

“…One of these receptors, L-selectin (CD62L), mediates the homing of leukocytes to LNs through binding to its carbohydrate ligands on the high endothelial venules. L-selectin is constitutively expressed by most leukocytes and does not require external, activating signals for function, although CD62L expression can be increased by certain activating factors (16). Unlike any other leukocyte adhesion proteins, CD62L is rapidly down-modulated from the cell surface following cell activation.…”