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IgG binding to cytoskeletal intermediate filaments activates the complement cascade.

G K Hansson, E Lagerstedt, A Bengtsson

    Experimental Cell Research
    |June 1, 1987
    PubMed
    Summary
    This summary is machine-generated.

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    Cell injury exposes cell interiors, causing IgG to bind intermediate filaments. This triggers complement activation via the classical pathway, generating mediators that may eliminate damaged cells.

    Area of Science:

    • Immunology
    • Cell Biology
    • Biochemistry

    Background:

    • Cellular plasma membrane damage increases permeability to macromolecules.
    • Following injury, IgG binds to intermediate filaments via its Fc portion.
    • This IgG binding is a potential early step in eliminating injured cells.

    Purpose of the Study:

    • To investigate the effect of IgG binding to intermediate filaments on the complement system.
    • To determine if intermediate filaments can activate the complement cascade.
    • To identify the role of complement activation in the cellular injury response.

    Main Methods:

    • Reconstituting intermediate filaments in vitro from purified vimentin.
    • Incubating filaments with plasma proteins and using cross-linker experiments to detect IgG binding.

    Related Experiment Videos

  • Utilizing immunofluorescence to detect IgG and complement factor Clq binding to cytoskeletons of cultured endothelial cells.
  • Measuring the production of complement cleavage fragments (C3a, C5a) and chemotactic activity.

    • Main Results:

    • Vimentin possesses an Fc-binding site for IgG heavy chains.
    • IgG binding to filaments in serum is accompanied by Clq binding.
    • Complement activation via the classical pathway (C4, C3 fixation) occurs on intermediate filaments.
    • Exposure of serum to filaments generates anaphylatoxic (C3a) and chemotactic (C5a) fragments.
    • C5a generation is dependent on C5 and the classical complement cascade.

    Conclusions:

    • Cellular damage leads to IgG binding to intermediate filaments and classical complement pathway activation.
    • This process generates bioactive mediators (C3a, C5a) that can recruit leukocytes and affect vascular permeability.
    • The described mechanism likely functions as a scavenger system for eliminating damaged cells.