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Updated: Aug 13, 2026

Determining the Phagocytic Activity of Clinical Antibody Samples
Published on: November 30, 2011
Persistence and selectivity of the immune phagocytosis inhibition by major histocompatibility complex antibodies
1Institute of Clinical Immunology and Blood Transfusion, Justus Liebig University, Giessen, FRG.
Major histocompatibility complex (MHC) antibodies induce immune phagocytosis inhibition (IPI) which lasts for at least 7 days. IPI-inducing antibodies do not inhibit the phagocytosis mediated by the beta-glucan receptor. This corresponds well to recent findings that these antibodies do not interfere with the phagocytosis of deactivated saccharomyces, mediated by the mannose-fucose receptor, or polyacrylic acid particles, also mediated by non-Fc receptors. Substances that interact with certain MHC antigens or with Fc receptors, certain toxins that inhibit surface molecule mobility, and ciclosporin do not cause IPI and do not suppress the induction of IPI by MHC antibodies. These substances are: opioid peptides, insulin, penicillin G, immune complexes, aggregated IgG, Fc fragments, ciclosporin, botulinum C2 toxin, sodium azide. Some lectins and EDTA are inhibitory in a non-selective fashion, since the Fc receptor independent phagocytosis is also abrogated.
Major histocompatibility complex (MHC) antibodies induce immune phagocytosis inhibition (IPI) which lasts for at least 7 days. IPI-inducing antibodies do not inhibit the phagocytosis mediated by the beta-glucan receptor. This corresponds well to recent findings that these antibodies do not interfere with the phagocytosis of deactivated saccharomyces, mediated by the mannose-fucose receptor, or polyacrylic acid particles, also mediated by non-Fc receptors. Substances that interact with certain MHC antigens or with Fc receptors, certain toxins that inhibit surface molecule mobility, and ciclosporin do not cause IPI and do not suppress the induction of IPI by MHC antibodies. These substances are: opioid peptides, insulin, penicillin G, immune complexes, aggregated IgG, Fc fragments, ciclosporin, botulinum C2 toxin, sodium azide. Some lectins and EDTA are inhibitory in a non-selective fashion, since the Fc receptor independent phagocytosis is also abrogated.
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