Open AccessIncreased adhesion of human monocytes to IL‐4‐stimulated human venous endothelial cells via CD11/CD18, and very late antigen‐4 (VLA‐4)/vascular cell adhesion molecule‐1 (VCAM‐Independent mechanisms
Author(s) -
VERDEGAAL E. M. E.,
BEEKHUIZEN H.,
BLOKLAND I.,
FURTH R.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb07982.x
Subject(s) - cell adhesion molecule , vcam 1 , cd18 , immunology , cell adhesion , adhesion , antigen , soluble cell adhesion molecules , biology , microbiology and biotechnology , chemistry , icam 1 , integrin alpha m , immune system , organic chemistry
SUMMARY Expression of adhesion molecules on endothelial cells (EC) can be up‐regulated or induced by cytokines. The aim of the present study was to investigate the effect of IL‐4on both the expression of adhesion molecules on EC and monocyte adhesion to EC. Flow cytometric analysis showed that VCAM‐1 expression on EC was up‐regulated after stimulation with IL‐4 for 24 h, whereas the expression of E‐selectin (formerly called endothelial leucocyte adhesion molecule‐1 (ELAM‐1)) was not enhanced, and that of intercellular adhesion molecule‐1 (ICAM‐1) only slightly. The adhesion of monocytes to EC increased to maximum values upon stimulation of EC with IL‐4 for 24 h. Coating of monocytes with MoAb against the integrin β 2 ‐subunit (CD18) significantly inhibited their adhesion to IL‐4‐stimulated EC; maximal inhibition was found when monocytes were coated with anti‐CD18 MoAb in combination with MoAb against CD49d (the α‐chain of VLA‐4), whereas no inhibition was found when monocytes were coated only with MoAb against CD49d. Monocyte adhesion was not significantly inhibited when IL‐4‐stimulated EC were coated with MoAbs against ICAM‐1 or VCAM‐1 alone or in combination. Adhesion of monocytes was inhibited to a greater extent when in addition to coating of monocytes with MoAb against CD18 the EC were coated with MoAb against VCAM‐1. From these results we conclude that monocytes bind to IL‐4‐stimulated EC via interaction of CD11/CD18 molecules on the monocytes with an as yet unknown endothelial ligand, and interaction of VLA‐4 on monocytes with VCAM‐1 on EC.