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

Olivier Spertini*, Geoffrey S. Kansas, J. Michael Munro, James D. Griffin, Thomas F. Tedder

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

228 Scopus citations

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 sites1-10. As lymphocytes and neutrophils express the same LAM-1 protein11,12, 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, PPME13-16, 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.

Original languageEnglish (US)
Pages (from-to)691-694
Number of pages4
JournalNature
Volume349
Issue number6311
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

  • General

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