SUMMARYWe have developed a pane! of MoAbs against four separate but overlapping epitopes on endothelial cell (EC) vascular cell adhesion molecule-I (VCAM-1). Two ofthe MoAbs (IG 11 and IH5) inhibited T cell adhesion to tumour necrosis factor (TN F)-activated EC. whilst two MoAbs (1.4C3 and 6D9) did not. Using these MoAbs we have identified acirculating form of VCAM-1 (cVCAM-l) which has identical epitope distribution to the EC form, and which is able to support the adhesion ofthe human lymphoblastoid cell line Jurkat J6 hy a VLA-4-and VCAM-1-dependent mechanism when immobilized from plasma. cVCAM-i isolated by immunoaffinity and size-exclusion chromatographies was shown by SDS-PAGE to have an apparent mot. wt of 85-90 kD. Levels of cVCAM-1 were significantly raised (P < 0 001) in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) compared with normal individuals. Il is possible thai cVCAM-l may be a useful plasma marker for the diagnosis and management ofpatients with inflammatory diseases. Furthermore, detection of elevated cVCAM-1 levels may act as a guide to the importance of VCAM-1-dependent cell adhesion in different pathological settings.
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