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© The Rockefeller University Press, 0022-1007/1996/12/2385/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2385-2392

Articles

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

Diana Sylvestre*, Raphael Clynes*, Minga Ma{ddagger}, Henry Warren{ddagger}, Michael C. Carroll{ddagger}, and Jeffrey V. Ravetch*

From the * Division of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York 10021; and {ddagger} 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 Fc{gamma}R receptors, but not complement, are required for antibody-triggered murine inflammatory responses.

Address correspondence to Jeffrey V. Ravetch at his present address, The Rockefeller University, 1230 York Avenue, New York, NY 10021.

These studies were supported by grants from the National Institutes of Health to M.C. Carroll and J.V. Ravetch, from the American Arthritis Foundation (to M.C. Carroll) by the DeWitt Wallace Foundation (to J.V. Ravetch) and by the Memorial Sloan-Kettering Cancer Center Clinical Scholars Program (to R. Clynes, National Cancer Institute grant CA-09512).

1Abbreviations used in this paper: ADCC, antibody-dependent cellular cytotoxicity; AIHA, autoimmune hemolytic anemia; ITP, immune thrombocytopenic purpura; MRBC, mouse RBC.

Diana Sylvestre and Raphael Clynes contributed equally to this work.


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