Abstract

Background:Inflammation in rheumatoid arthritis (RA) is caused by multiple cell types, including infiltrating inflammatory cells, such as lymphocytes, neutrophils, macrophages, and spindle-shaped fibroblasts. Especially, we are focusing on fibroblast-like synoviocytes (FLSs). In our previous study, we have reported that FLSs were positive for multiple markers including CD14, CD68 and HLA-DR, and were dendritic-shaped cells constituting nursing phenomenon between lymph or plasma cells. In addition, in our recent study, we found that CD14+FLSs were positive for vimentin (VIM), which is a marker for mesenchymal cells. There are still many issues to be discussed regarding CD14+VIM+ cells.Objectives:To investigate the relationship between CD14+VIM+ cells and the degree of synovitis in rheumatoid arthritis.Methods:Synovial tissues collected from RA patients who underwent joint surgeries were prepared for this study. First, the proportions of CD14+ cells in RA synovial tissue and control were analyzed using flow cytometry and the concentrations of inflammatory cytokines released by CD14+ cells in RA synovial tissue and control were examined by ELISA. Next, the proportions of CD14+VIM+ cells in RA synovial tissue and control were examined immunohistologically and then we analyzed the results using image analysis software. Also, we statistically analyzed the relationship between the proportion of CD14+VIM+ cells, the degree of synovitis, and clinical data.Results:Results of flow cytometry showed that CD14+ cells were frequently observed in RA synovial tissue than control. Cultured CD14+ cells released more inflammatory cytokines than cultured CD14- cells. Also, results of immunohistological staining showed that many CD14+VIM+ cells were observed in RA synovial tissue than in control. The proportion of CD14+VIM+ cells was correlated with Krenn synovitis score. High proportion cases significantly showed high level of CRP and MMP-3.Conclusion:CD14+VIM+ cells might be involved in the mechanism of chronic immunological inflammation in RA and the proportion of these cells might influence the clinical data.

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