F M Cicuttini1, M Martin, A W Boyd. 1. Lions Clinical Cancer Research Laboratory, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Australia.
Abstract
OBJECTIVES: To study the role of cytokines on adhesion molecule expression and binding of activated T cells to synovial type B cells. METHODS: Adhesion molecule expression was examined by immunofluorescence and adhesion of 51Cr-labelled T cells to the synovial cells determined. RESULTS: Tumor necrosis factor alpha/interferon gamma (TNF alpha/IFN-gamma) and interleukin 1 alpha (IL-1 alpha)/IFN-gamma enhanced adhesion molecule expression and the adhesion of T cells to synovial cells. Anti-intercellular adhesion molecule 1 blocked adhesion of T cells to TNF alpha/IFN-gamma and IL-1 alpha/IFN-gamma stimulated synovial cells while an antibody to CD61 blocked adhesion to IL-1 alpha/IFN-gamma stimulated cells. CONCLUSIONS: The interaction of leukocytes with adhesion molecules on synovial cells may play a role in recruitment of these cells to an inflammatory site.
OBJECTIVES: To study the role of cytokines on adhesion molecule expression and binding of activated T cells to synovial type B cells. METHODS: Adhesion molecule expression was examined by immunofluorescence and adhesion of 51Cr-labelled T cells to the synovial cells determined. RESULTS:Tumor necrosis factor alpha/interferon gamma (TNF alpha/IFN-gamma) and interleukin 1 alpha (IL-1 alpha)/IFN-gamma enhanced adhesion molecule expression and the adhesion of T cells to synovial cells. Anti-intercellular adhesion molecule 1 blocked adhesion of T cells to TNF alpha/IFN-gamma and IL-1 alpha/IFN-gamma stimulated synovial cells while an antibody to CD61 blocked adhesion to IL-1 alpha/IFN-gamma stimulated cells. CONCLUSIONS: The interaction of leukocytes with adhesion molecules on synovial cells may play a role in recruitment of these cells to an inflammatory site.