Upregulated expression of CCR3 in rheumatoid arthritis and CCR3-dependent activation of fibroblast-like synoviocytes.

摘要: It is recognized that CC chemokine receptor 3 (CCR3) associated with numerous inflammatory conditions and fibroblast-like synoviocyte (FLS) invasiveness correlates articular damage in rheumatoid arthritis (RA). However, little known of the expression action CCR3 on FLS RA. In present study, we investigated dispersed synovial tissue peripheral blood cells RA influence eotaxin-1 functions by using flow cytometry analysis, challenge, real-time PCR techniques. The results showed approximately 7.0 % are CCR3+ cells. Among those cells, 38.1, 23.8, 20.6 CD90+CD14−CD3− (representing FLS), CD14+, CD8+ respectively, indicating one major populations blood, CD14+ elevated, but CD8+CCR3+ reduced was found induced upregulated matrix metalloproteinase (MMP)-9 messenger RNAs (mRNAs) FLS. Since an antagonist suppressed eotaxin-1, event appeared dependent. Moreover, observed interleukin (IL)-1β markedly enhanced release from FLS, TNF-α at 12 24 h following incubation. conclusion, increased levels plasma fluid (SF) indicate CCR3-mediated mechanisms may play important role Blockage provoked MMP-9 CCR3, implicating anti-CCR3 agents have therapeutic use for