IMMUNOGLOBULIN G-MEDIATED INFLAMMATORY RESPONSES DEVELOP NORMALLY IN COMPLEMENT-DEFICIENT MICE

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 t hese mice have types II and III inflammatory responses that are indist inguishable 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 a ntiplatelet antibodies. Furthermore, in the reverse passive Arthus rea ction, soluble immune complexes induce equivalent levels of hemmorhage , edema, and neutrophillic infiltration in complement-deficient and wi ld-type animals. In contrast, mice that are genetically deficient in t he 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 gamma R r eceptors, but not complement, are required for antibody-triggered muri ne inflammatory responses.