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Related Experiment Videos

Complement activation induced by rabbit rheumatoid factor

R R Meyer, J C Brown

    Infection and Immunity
    |July 1, 1980
    PubMed
    Summary
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    Rabbit rheumatoid factor, identified in anti-streptococcal serum, activates complement and causes red blood cell lysis. This factor shows preferential binding to rabbit immunoglobulin G, impacting hemolytic activity.

    Area of Science:

    • Immunology
    • Rheumatology

    Background:

    • Rheumatoid factor (RF) is an autoantibody that targets the Fc region of immunoglobulin G (IgG).
    • Understanding RF's interaction with complement and its specific binding properties is crucial for autoimmune disease research.

    Purpose of the Study:

    • To characterize the hemolytic activity of rabbit rheumatoid factor (RRF).
    • To investigate the binding specificity of RRF to different immunoglobulin G fragments.

    Main Methods:

    • Hyperimmunization of rabbits with streptococcal vaccine to produce anti-streptococcal serum.
    • Fractionation of serum using Sephacryl S-200 chromatography.
    • Hemolytic assays using antibody-coated erythrocytes and complement.
    • Hemolytic inhibition assays with various immunoglobulin G fragments (Fc, Fab, F(ab')2).

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  • Plaque-forming cell assays to enumerate antibody-forming cells.

    • Main Results:

    • Both 19S and 7S fractions of anti-streptococcal serum exhibited hemolytic activity.
    • Hemolysis was dependent on complement activation.
    • Rabbit rheumatoid factor was confirmed as the cause of hemolysis through inhibition assays.
    • RRF showed preferential reactivity towards rabbit immunoglobulin G, particularly the Fc region.
    • Immunoglobulin G-specific antibody-forming cells were detected in spleen and peripheral blood lymphocytes.

    Conclusions:

    • Rabbit rheumatoid factor possesses complement-activating and hemolytic properties.
    • RRF exhibits specific binding affinity for rabbit immunoglobulin G.
    • The study provides insights into the mechanisms of RF-mediated hemolysis and cellular immune responses.