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From the * Division of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York
10021; and The role of complement in immunoglobulin G-triggered inflammation was studied in mice
genetically deficient in complement components C3 and C4. Using the reverse passive Arthus
reaction and experimental models of immune hemolytic anemia and immune thrombocytopenia, we show that these mice have types II and III inflammatory responses that are indistinguishable from those of wild-type animals. Complement-deficient and wild-type animals exhibit comparable levels of erythrophagocytosis and platelet clearance in response to cytotoxic
anti-red blood cell and antiplatelet antibodies. Furthermore, in the reverse passive Arthus reaction, soluble immune complexes induce equivalent levels of hemmorhage, edema, and neutrophillic infiltration in complement-deficient and wild-type animals. In contrast, mice that are
genetically deficient in the expression of Fc receptors exhibit grossly diminished reactions by
both cytotoxic antibodies and soluble immune complexes. These studies provide strong evidence that the activation of cell-based Fc
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115
R receptors, but not complement, are required for
antibody-triggered murine inflammatory responses.
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