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Relative contribution of the leukocyte molecules MO1, LFA‐1, and p150,95 (LeuM5) in adhesion of granulocytes and monocytes to vascular endothelium is tissue‐ and stimulus‐specific
Author(s) -
Arnaout M. Amin,
Lanier Lewis L.,
Faller Douglas V.
Publication year - 1988
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041370214
Subject(s) - umbilical vein , biology , cell adhesion molecule , granulocyte , monocyte , adhesion , endothelium , microbiology and biotechnology , cell adhesion , lymphocyte function associated antigen 1 , monoclonal antibody , endothelial stem cell , immunology , intercellular adhesion molecule 1 , in vitro , biochemistry , antibody , chemistry , cell , endocrinology , organic chemistry
Adhesion of human monocytes and granulocytes to vascular endothelium plays an important role in migration of these cells to inflammatory sites in tissues. A family of three human leukocyte heterodimeric surface molecules named Mo1, LFA‐1, and p150,95 (LeuM5) has been shown to mediate leukocyte adhesion to confluent monolayers of human umbilical vein endothelial cells (HUVE). The relative contribution of each of the three molecules in leukocyte endothelial adhesion was studied using a variety of stimuli. Purified human granulocytes and monocytes were radiolabelled and incubated with HUVE for 45 minutes in a 37°C humidified 5% CO 2 incubator in the presence or absence of subunit‐specific monoclonal antibodies (MAbs). Adhesion was assessed by quantitation of endothelial cell‐associated radioactivity and confirmed by microscopic evaluation. MAbs directed against the alpha subunit of LFA‐1 as well as to the beta subunit common to all three antigens significantly inhibited unstimulated monocyte adhesion to HUVE. Small but significant inhibition was also observed using MAbs directed against Mo1 a and p150. Phorbol myristate acetate (PMA)‐induced grranulocyte adhesion to HUVE was significantly inhibited by anti‐Mo1 a and anti‐beta, but not by anti‐LFA‐1 a or anti‐p150. When HUVE were prestimulated by recombinant IL‐1, a different pattern of antigen utilization by granulocytes was observed. MAbs directed against each of the three alpha subunits as well as the common beta subunit all inhibited granulocyte adhesion to HUVE. Furthermore the effect of the three anti‐alpha subunit MAbs on granulocyte‐HUVE adhesion was additive. These studies show that relative contribution of Mo1, LFA‐1, and p150,95 to leukocyte endothelial adhesion varies depending on the cell type and the stimulus used. These studies also reveal a novel role for p150,95 in promoting monocyte and granulocyte adhesion to HUVE.