Open AccessEffect of cytokine‐induced soluble ICAM‐1 from human synovial cells on synovial cell‐lymphocyte adhesion
Author(s) -
SHINGU M.,
HASHIMOTO M.,
EZAKI I.,
NOBUNAGA M.
Publication year - 1994
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.1365-2249.1994.tb06605.x
Subject(s) - cytokine , synovitis , icam 1 , lymphocyte , cell adhesion , immunology , biology , monoclonal antibody , synovial membrane , cell adhesion molecule , cell culture , adhesion , microbiology and biotechnology , cell , chemistry , inflammation , antibody , arthritis , biochemistry , genetics , organic chemistry
SUMMARY The present study was designed to establish (i) the effects of cytokines on soluble ICAM‐1 (sICAM‐1) production by human synovial cells (SC) and ICAM‐1 expression on these cells, and (ii) the effects of sICAM‐1 on lymphocyte‐SC adhesion. sICAM‐1 production was enhanced in parallel with ICAM‐1 expression by IL‐1β, TNF‐α and IFN‐γ. IL‐4 showed no effects on ICAM‐1 expression. In contrast with the transient elevation of cell‐associated ICAM‐1 by IL‐1β, which peaked 36 h after stimulation and declined thereafter, sICAM‐1 continued to accumulate in culture supernatants even after 48 h. Purified sICAM‐1 was obtained from a 48h culture synovial cell supernatant by affinity chromatography using ICAM‐1 monoclonal antibody. The purified sICAM‐1 significantly inhibited adhesion of lymphocytes and monocytes to cytokine‐stimulated synovial cells. These results suggest that sICAM‐1 may modulate chronic synovitis by inhibiting ICAM‐1‐mediated cell‐to‐cell adhesion.