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Alternative pathway complement activation in rheumatoid arthritis
Insights
Rheumatoid arthritis (RA) shows increased alternative pathway complement turnover, indicated by lower factor B and properdin levels in synovial fluid. However, C3b inactivator levels were reduced, suggesting it doesn't control this pathway's activity in RA.
Area of Science:
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation.
- The complement system, particularly the alternative pathway, plays a role in RA pathogenesis.
- Understanding complement component levels in synovial fluid is crucial for RA research.
Purpose of the Study:
- To investigate the levels of complement components in the synovial fluid of RA patients.
- To determine the involvement of the alternative complement pathway in RA.
- To assess the role of C3b inactivator and beta 1H in regulating complement turnover in RA.
Main Methods:
- Measurement of serum and synovial fluid (SF) complement components (C3, C5, factor B, properdin, beta 1H, C3b inactivator).
- Quantification of SF C3d and Ba concentrations.
- Comparison of levels between 40 RA patients and 5 osteoarthritis patients.
Main Results:
- Decreased SF concentrations of factor B and properdin were observed in RA patients.
- Increased SF Ba levels indicated enhanced alternative pathway turnover in RA.
- Reduced SF C3b inactivator concentrations were found, while beta 1H levels remained unchanged.
Conclusions:
- Increased alternative pathway turnover occurs in rheumatoid arthritis.
- Alternative pathway turnover in RA is dependent on C3 turnover.
- Reduced C3b inactivator levels in RA do not appear to control alternative pathway turnover.
Abstract:
Serum and synovial fluid (SF) levels of the complement components C3, C5, factor B (B), properdin (P), beta 1H and C3b inactivator (C3bINA), and EDTA-plasma and SF concentrations of C3d and Ba were measured in 40 rheumatoid arthritis (RA) and 5 patients with osteoarthritis. Decreased SF concentration of B and P and increased levels of Ba showed that increased alternative pathway turnover occurred in RA. Reduced SF C3bINA concentrations occurred, but levels of beta 1H were not reduced. The results showed that alternative pathway turnover was dependent upon C3 turnover, but failed to support the notion that levels of C3bINA or beta 1H control alternative pathway turnover in RA.