The Journal of Experimental Medicine
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J. Exp. Med.
© The Rockefeller University Press
0022-1007/96/12/2385/08 $2.00
Volume 184 December 1996 2385-2392

Immunoglobulin G-mediated Inflammatory Responses Develop Normally in Complement-deficient Mice

By Diana Sylvestre,* Raphael Clynes,* Minga Ma,Dagger Henry Warren,Dagger Michael C. Carroll,Dagger and Jeffrey V. Ravetch*

From the * Division of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York 10021; and Dagger  Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

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 Fcgamma R receptors, but not complement, are required for antibody-triggered murine inflammatory responses.


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