Open AccessExpression of decay‐accelerating factor is reduced on hyperplastic synovial lining cells in rheumatoid synovitis
Author(s) -
ITOH J.,
NOSE M.,
FUJITA T.,
KATO M.,
OHYAMA A.,
KYOGOKU M.
Publication year - 1991
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.1365-2249.1991.tb05644.x
Subject(s) - synovitis , synovial membrane , decay accelerating factor , immunology , rheumatoid factor , antibody , synovial fluid , monoclonal antibody , inflammation , pathology , rheumatoid arthritis , complement system , biology , chemistry , medicine , osteoarthritis , alternative medicine
SUMMARY Decay‐accelerating factor (DAF), a membrane inhibitor of homologous complement activation, is present in synovial cells liningjoint space and detected in synovial fluid. DAF is considered to protect synovial membrane from complement‐mediated injury associated with articular inflammation. We studied the immunohistopathological features of DAF molecules in synovial membrane of rheumatoid synovitis using a DAF‐specific monoclonal antibody, IC6. Reacting molecules with the 1C6 antibodies in synovial tissue extracts formed a 70‐kD band in Western blot analysis. DAF was strongly detected on the flat synovial lining cells, but weakly on the hyperplastic and multi‐layered lining cells in rheumatoid synovitis. The latter cells reacted with anti‐Lcu‐M3 antibodies specific for a cell surface marker of activated macrophages, sometimes accompanied by C3 and IgM deposition on the superficial synovial membrane. These results suggest that active rheumatoid synovitis characteristically with hyperplastic synovial lining cells is out of control by DAF, thereby permitting further complement‐mediated injury.