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

• Published in: Nature (London) 1991-02, Vol.349 (6311), p.691-694
• Main Authors: Spertini, Olivier, Kansas, Geoffrey S, Munro, J. Michael, Griffin, James D, Tedder, Thomas F
• Format: Article
• Language: English
• Subjects: Adhesion; Affinity; Antibodies, Monoclonal; Antigens, Differentiation, T-Lymphocyte; Binding; Biological and medical sciences; Carbohydrates; CD2 Antigens; Cell activation; Cell Adhesion - drug effects; Cell Adhesion - physiology; Cell Adhesion Molecules - metabolism; Cell Movement - physiology; Cellular biology; Cross-Linking Reagents; Edetic Acid - pharmacology; Endothelium; Endothelium, Vascular - metabolism; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Granulocyte Colony-Stimulating Factor - physiology; Granulocyte-Macrophage Colony-Stimulating Factor - physiology; Granulocytes; Humans; Immunobiology; Immunoglobulins; Inflammation; L-Selectin; Leukocyte migration; Leukocytes; Leukocytes (neutrophilic); Ligands; Lymph nodes; Lymphocyte Activation; Lymphocytes; Lymphocytes - drug effects; Lymphocytes - metabolism; Mannans - metabolism; Mannosephosphates - metabolism; Medical research; Modulation of the immune response (stimulation, suppression); Molecules; Neutrophils; Neutrophils - drug effects; Neutrophils - metabolism; Receptors, Immunologic; Signal transduction; Stimuli; T-Lymphocytes - metabolism
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/349691a0

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.