Open AccessDetection of a circulating form of vascular cell adhesion molecule‐1: raised levels in rheumatoid arthritis and systemic lupus erythematosus
Author(s) -
WELLICOME S. M.,
KAPAHI P.,
MASON J. C.,
LEBRANCHU Y.,
YARWOOD H.,
HASKARD D. O.
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.tb03413.x
Subject(s) - rheumatoid arthritis , immunology , cell adhesion molecule , cell adhesion , epitope , lupus erythematosus , medicine , tumor necrosis factor alpha , adhesion , cell , antibody , chemistry , biochemistry , organic chemistry
SUMMARY We have developed a panel of MoAbs against four separate but overlapping epitopes on endothclial cell (EC) vascular cell adhesion molecule‐1 (VCAM‐1). Two of the MoAbs(1G11 and IE5) inhibited T cell adhesion to tumour necrosis factor (TNF)‐activated EC, whilst two MoAbs (1.4C3 and 6D9) did not. Using these MoAbs we have identified a circulating form of VCAM‐1 (cVCAM‐l) which has identical epitope distribution to the EC form, and which is able to support the adhesion of the human lymphoblastoid cell line Jurkat J6 by a VLA‐4‐ and VCAM‐1‐dependent mechanism when immobilized from plasma. cVCAM‐l isolated by immunoaffinity and size‐exclusion chromatographies was shown by SDS‐PAGE to have an apparent mol. wt of 85 90 kD. Levels of cVCAM‐l were significantly raised ( P < 0.001) in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) compared with normal individuals. It is possible that cVCAM‐l may be a useful plasma marker for the diagnosis and management of patients with inflammatory diseases. Furthermore, detection of elevated cVCAM‐l levels may act as a guide to the importance of VCAM‐1‐dependent cell adhesion in different pathological settings.