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Complement-dependent immunoglobulin G receptor function in lymphoid cells.

J C Scornik

    Science (New York, N.Y.)
    |May 7, 1976
    PubMed
    Summary
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    Antibody-coated cells are usually not destroyed by lymphoid cells due to blocked receptors. However, complement activation unblocks these receptors, allowing cell destruction even with normal immunoglobulin G (IgG) present.

    Area of Science:

    • Immunology
    • Cellular Biology
    • Complement System

    Background:

    • Lymphoid cells mediate antibody-dependent cell-mediated cytotoxicity (ADCC).
    • Normal immunoglobulin G (IgG) typically blocks IgG receptors on lymphoid cells, inhibiting ADCC.
    • The role of IgG receptors in vivo, considering high serum IgG levels, remains unclear.

    Purpose of the Study:

    • To investigate the mechanism of IgG receptor unblocking in ADCC.
    • To determine if ADCC can occur in the presence of normal IgG under specific conditions.
    • To elucidate the in vivo relevance of IgG receptors despite high IgG concentrations.

    Main Methods:

    • Utilizing in vitro assays to assess lymphoid cell cytotoxicity against antibody-coated target cells.
    • Manipulating target cell sensitization with antibodies and complement.

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  • Quantifying cytotoxicity in the presence of varying concentrations of normal IgG.

    • Main Results:

    • Lymphoid cells showed inhibited lysis of antibody-coated target cells with normal IgG.
    • Cytotoxicity was restored when target cells were sensitized with antibodies and complement, even with normal IgG present.
    • Complement-mediated unblocking of IgG receptors facilitates ADCC.

    Conclusions:

    • IgG receptors can function in vivo for cell-mediated cytotoxicity.
    • Complement activation plays a crucial role in overcoming IgG-mediated receptor blockade.
    • This mechanism allows for effective immune surveillance and target cell elimination in environments with high IgG concentrations.