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Terminal complement complexes and C1/C1 inhibitor complexes in rheumatoid arthritis and other arthritic conditions
D A Oleesky1, R H Daniels, B D Williams
1Department of Medical Biochemistry, University Hospital of Wales, Heath Park, Cardiff.
Insights
Complement activation markers, terminal complement complex (TCC) and C1r-C1s-C1 inhibitor complex (C1/C1 INH), are elevated in rheumatoid arthritis (RA) patients, indicating a role in disease pathogenesis.
Area of Science:
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) involves complex immunological pathways.
- The complement system plays a role in inflammatory and autoimmune diseases.
Purpose of the Study:
- To investigate the concentrations of terminal complement complex (TCC) and C1r-C1s-C1 inhibitor complex (C1/C1 INH) in patients with arthritis.
- To correlate these complement markers with disease activity measures in rheumatoid arthritis.
Main Methods:
- Measurement of TCC and C1/C1 INH in plasma and synovial fluid.
- Comparison of concentrations between rheumatoid arthritis, osteoarthritis, and healthy individuals.
- Correlation analysis with IgM rheumatoid factor, immune complexes, and disease severity scores.
Main Results:
- TCC and C1/C1 INH concentrations were significantly higher in RA patients compared to osteoarthritis patients and healthy controls.
- No significant correlation was found between TCC levels and other markers in RA patients.
- A significant correlation between C1/C1 INH and immune complexes was observed in the synovial fluid of seronegative RA patients.
- Complement marker concentrations did not correlate with disease severity (Ritchie score).
Conclusions:
- Complement activation is confirmed to be involved in rheumatoid arthritis pathogenesis.
- Multiple mechanisms likely contribute to the inflammatory processes in RA.
- Specific complement components may have distinct roles depending on disease subset or location.
Abstract:
Terminal complement complex (TCC) and C1r-C1s-C1 inhibitor complex (C1/C1 INH) concentrations were measured in plasma and synovial fluid from patients with arthritis and related to other measures of disease activity. Both TCC and C1/C1 INH concentrations were significantly increased in patients with rheumatoid arthritis (RA) compared with patients with osteoarthritis (plasma and synovial fluid, P less than 0.05) and normal subjects (plasma only, P less than 0.001). In the patients with RA, there was no correlation between plasma or synovial fluid TCC concentrations and IgM rheumatoid factor, immune complex or C1/C1 INH levels. However, in 10 patients with seronegative RA, C1/C1 INH and immune complex levels correlated significantly in synovial fluid (r = 0.69, P less than 0.05) although not in plasma (r = 0.52). Plasma and synovial fluid TCC and C1/C1 INH concentrations did not differ in rheumatoid patients with severe compared with mild joint disease (categorized by the Ritchie score). These results confirm a role for complement activation in RA but suggest that several mechanisms are involved in its pathogenesis.