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Complement-induced ultrastructural membrane lesions: requirement for terminal components

C H Packman, S I Rosenfeld, R I Weed

    Journal of Immunology (Baltimore, Md. : 1950)
    |November 1, 1976
    PubMed
    Summary
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    Complement ring lesions on erythrocytes require later complement components beyond C5. Studies using complement-deficient sera show C5 binding alone doesn

    Area of Science:

    • Immunology
    • Cell Biology

    Background:

    • The formation of complement (C)-induced ring lesions on antibody-coated erythrocytes (EA) is a key indicator of complement system activation.
    • The precise step in the complement cascade where these 8- to 11-nm ring lesions appear has been a subject of ongoing debate.
    • Previous research has yielded conflicting conclusions regarding whether lesions form at the C5 step or require later components like C8 and C9.

    Purpose of the Study:

    • To definitively determine the complement sequence step at which ring-shaped lesions form on antibody-coated erythrocytes.
    • To investigate the relationship between C5 binding and the ultrastructural formation of complement-induced ring lesions.
    • To clarify the complement requirements for ring lesion formation in relation to cell lysis.

    Main Methods:

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  • Utilized sheep antibody-coated erythrocytes (EA) and human sera genetically deficient in specific complement components (C5, C6, C7, or C8).
  • Examined negatively stained erythrocyte membranes using electron microscopy (x 220,000) in a blinded manner.
  • Correlated the observed ring lesion density with quantitative measurements of 125I-C5 binding to EA.

    • Main Results:

    • Rare ring lesions were observed on EA exposed to sera lacking C5, C6, C7, or C8, and heated normal serum, with minimal lesion density.
    • Fresh normal serum (NHS) induced significantly higher lesion densities (140–220/µm²).
    • While C5 binding varied in deficient sera, even enhanced C5 binding (with iodine treatment) did not increase lesion formation unless later complement components were present.

    Conclusions:

    • Complement C5 binding to erythrocytes is insufficient for the formation of ultrastructural ring lesions in the absence of later-acting complement components (at least through C8).
    • The formation of complement-induced ring lesions requires the action of terminal complement components, similar to the requirements for erythrocyte lysis.
    • These findings resolve the controversy by demonstrating that ring lesions are not solely a C5-mediated event but depend on the complete complement cascade.