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The ability of the Fc fragment to trigger an immune injury to human platelets challenged with immune complexes or aggregated IgG was mainly observed in plasma-free medium. We now report immune injury to human platelets in autologous plasma when Protein A-bearing staphylococci were added to the system. Protein A, a cell wall constituent of pathogenic staphylococci interacts with the Fc fragment of IgG making it reactive with the membrane receptor. Aggregation amd release of [3H]serotonin from human platelets suspended in autologous plasma occured when at least two Protein A-bearing staphylococci were added per one platelet. Partial stripping of Protein A by trypsinization reduced the extent of platelet injury. When Protein A was solubilized and isolated by affinity chromatography, release of [3H]serotonin by soluble Protein A-IgG complexes occured only in plasma-free medium. Using radiolabelled Protein A, we demonstrated that release of [3H]serotonin was paralleled by the binding of [125I]Protein A-IgG complexes to platelet membrane. This binding was dependent on the Fc fragment and its receptor since the removal of the Fc fragment abolished the binding of Protein A to platelets.Thus, immune injury to human platelets has been demonstrated in two systems: (1) when Protein A was in solid phase, i.e., attached to staphylococci, platelet injury by Protein A-IgG occured in plasma, and (2) when Protein A was in fluid phase, i.e., isolated from staphylococci, injury occured only in plasma-free medium. Both mechanisms required the Fc fragment of IgG to interact with the membrane receptor on human platelets.

The Role Of Fc Fragment Receptor in Immune Injury of Human Platelets Induced by Protein a of Staphylococci