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Related Experiment Videos

Complement fixation by small, DNase-resistant DNA-anti-DNA immune complexes.

C Horgan, W Emlen

    Molecular Immunology
    |February 1, 1987
    PubMed
    Summary
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    Immune complexes (IC) containing DNA fragments and IgG can activate complement. However, smaller ICs, even with complement component C3b, may not bind to red blood cells (RBCs), potentially persisting in circulation.

    Area of Science:

    • Immunology
    • Molecular Biology
    • Rheumatology

    Background:

    • Immune complexes (IC) play a role in autoimmune diseases like systemic lupus erythematosus (SLE).
    • The interaction between DNA-anti-DNA ICs, complement, and red blood cells (RBCs) influences their clearance and potential pathogenicity.

    Purpose of the Study:

    • To investigate the relationship between the size of DNase-treated DNA-anti-DNA immune complexes (IC) and their ability to incorporate complement component C3b and bind to complement receptor 1 (CR1) on RBCs.
    • To understand how IC size affects their clearance mechanisms and potential role in SLE pathogenesis.

    Main Methods:

    • Formation of 125I-ds DNA-anti-DNA ICs at antibody excess.
    • Treatment of ICs with DNase to generate smaller, DNase-resistant ICs.
    • Fractionation of DNase-treated ICs by sucrose density gradient (SDG) ultracentrifugation.

    Related Experiment Videos

  • Analysis of IC size, C3b incorporation, and RBC binding using autoradiography, electrophoresis, and functional assays.

    • Main Results:

    • ICs with one IgG molecule per DNA fragment (9-11S) showed neither C3b incorporation nor RBC binding.
    • ICs with up to four IgG molecules per DNA fragment (12-22S) showed increasing C3b incorporation with size but limited RBC binding.
    • ICs with four or more IgGs (22-24S) incorporated C3b and bound to RBCs effectively.
    • ICs containing three to four IgG molecules per DNA fragment were large enough to incorporate C3b but too small to bind efficiently to RBC CR1.

    Conclusions:

    • DNase-treated ICs of specific sizes can incorporate C3b but may evade clearance by RBC CR1.
    • These smaller, potentially persistent ICs could contribute to the pathogenesis of SLE.
    • Understanding IC size-dependent interactions is crucial for elucidating autoimmune disease mechanisms.