Effect of lymphocyte activation status on binding to endothelium. The role of CD11a, CD18 and CD49d adhesion molecules.
When endothelial cells (EC) were stimulated with IL-1 and/or lymphocytes with rIL-2 or PHA, the binding of lymphocytes to EC was increased. PMA treatment of lymphocytes alone did not increase their binding to EC, but when EC were additionally induced with IL-1 the binding was increased. The expression of LFA-1 was constant, whilst the expression of CD49d was increased after rIL-2 and PHA stimulation. The PMA- and rIL-2-induced lymphocyte binding to IL-1-induced EC was inhibited by anti-CD11a, CD18 and CD49d mAbs; on the other hand, the enhanced binding of PHA-stimulated lymphocytes to EC could not be blocked by these mAbs. These results show that activation of lymphocytes by various stimuli leads to different usage of adhesion pathways in their binding to inflammatory EC.
Turunen
J P
JP
Transplantation Laboratory, University of Helsinki, Finland.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D018845:CD11 Antigens / Q000096:biosynthesis* / Q000276:immunology; D018821:CD18 Antigens / Q000096:biosynthesis* / Q000276:immunology; D002448:Cell Adhesion / Q000187:drug effects; D004727:Endothelium / Q000166:cytology* / Q000187:drug effects; D005434:Flow Cytometry; D007375:Interleukin-1 / Q000494:pharmacology*; D007376:Interleukin-2 / Q000494:pharmacology*; D008214:Lymphocytes / Q000166:cytology* / Q000187:drug effects; D010835:Phytohemagglutinins / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011994:Recombinant Proteins / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D018845:CD11 Antigens; D018821:CD18 Antigens; D007375:Interleukin-1; D007376:Interleukin-2; D010835:Phytohemagglutinins; D011994:Recombinant Proteins; D013755:Tetradecanoylphorbol Acetate