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Experimental acantholysis by complement-fixing intercellular antibodies

T Hashimoto, M Sugiura, S Kurihara

    Archives of Dermatological Research
    |January 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

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    Complement-fixing intercellular antibodies in pemphigus sera bind to skin cells. However, complement is not essential for the observed acantholysis (skin blistering) in this in vitro study.

    Area of Science:

    • Immunodermatology
    • Autoimmune Blistering Diseases

    Background:

    • Pemphigus is an autoimmune disease characterized by autoantibodies targeting intercellular substances in the epidermis.
    • The role of complement activation in pemphigus pathogenesis remains incompletely understood.

    Purpose of the Study:

    • To investigate the role of complement in pemphigus pathogenesis using an organ culture system.
    • To determine if complement fixation by intercellular antibodies contributes to acantholysis in vitro.

    Main Methods:

    • Sera from untreated pemphigus patients with complement-fixing intercellular antibodies were used.
    • Organ culture of human skin was performed with these sera.
    • Immunofluorescence for IgG and C3 deposition was assessed.
    • Acantholysis-like changes were evaluated in complement-depleted and complement-supplied systems.

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    Main Results:

    • Complement-fixing intercellular antibodies showed IgG binding to the intercellular substance in organ-cultured skin.
    • Acantholysis-like changes were observed in 8 out of 10 cases.
    • C3 deposition was not detected initially.
    • Complement fixation was confirmed after adding fresh human serum.
    • No significant difference in acantholysis was noted between complement-depleted and supplied systems.

    Conclusions:

    • While complement-fixing intercellular antibodies are present in pemphigus sera, complement activation does not appear to be a necessary factor for inducing acantholysis in this in vitro organ culture model.