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Alternative pathway complement activation in rheumatoid arthritis.

A El-Ghobarey, K Whaley

    The Journal of Rheumatology
    |July 1, 1980
    PubMed
    Summary
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    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.

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  • 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.