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Complement components, C1 activation and disease activity in SLE.

G Sturfelt, A G Sjöholm, B Svensson

    International Archives of Allergy and Applied Immunology
    |January 1, 1983
    PubMed
    Summary
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    Systemic lupus erythematosus (SLE) involves complement system activation, particularly the classical pathway, indicated by decreased C1q, C4, and C3 levels during active disease. Complement activation is independent of disease activity.

    Area of Science:

    • Immunology
    • Rheumatology
    • Clinical Chemistry

    Background:

    • Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune complex deposition and inflammation.
    • The complement system plays a crucial role in SLE pathogenesis, but its precise activation pathways and markers require further elucidation.

    Purpose of the Study:

    • To investigate laboratory parameters, focusing on complement system activation, in SLE patients during active and inactive disease states.
    • To correlate complement component levels with disease activity and renal manifestations.

    Main Methods:

    • Analysis of serum samples from 8 SLE patients during high and low disease activity periods.
    • Measurement of complement components (C1q, C4, C3, C2, C1r-C1s-C1 inactivator complexes, factor B, I, H, D), C-reactive protein, and immune complexes.

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  • Utilized both immunochemical and functional assays for complement components.

    • Main Results:

    • Elevated C1r-C1s-C1 inactivator complexes (C1r-C1s-Cl IA) indicated C1 activation, independent of disease activity.
    • During active SLE, decreased levels of C1q, C4, C3, and functional C2 suggested classical pathway activation.
    • Correlations were observed between C1r-C1s-Cl IA and C1q binding immune complexes in solid-phase assays.

    Conclusions:

    • The classical complement pathway is sequentially activated in active SLE.
    • Complement activation, evidenced by C1r-C1s-Cl IA, occurs independently of disease flares.
    • Further research is needed to understand the role of specific complement factors in SLE, particularly in cases with renal involvement.