DIVERGENT ROLES FOR Fc RECEPTORS AND COMPLEMENT IN VIVO

Recent results obtained in mice deficient in either FcRs or complement have revealed distinct functions for these two classes of molecules. While each is capable of interacting with antibodies or immune complexes, the two systems mediate distinct biological effector responses. Complement-deficient m...

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Bibliographic Details
Published in:Annual review of immunology 1998-01, Vol.16 (1), p.421-432
Main Authors: Ravetch, Jeffrey V, Clynes, Raphael A
Format: Article
Language:English
Subjects:
anaphylaxis
Animals
Complement System Proteins - physiology
glomerulonephritis
Humans
immune complex
inflammation
innate immunity
Mice
Receptors, Fc - physiology
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Summary:Recent results obtained in mice deficient in either FcRs or complement have revealed distinct functions for these two classes of molecules. While each is capable of interacting with antibodies or immune complexes, the two systems mediate distinct biological effector responses. Complement-deficient mice are unable to mediate innate immune responses to several bacterial pathogens and bacterial toxins, yet respond normally to the presence of cytotoxic antibodies and pathogenic immune complexes. In contrast, FcR-deficient mice display no defects in innate immunity or susceptibility to a variety of pathogens, yet they are unable to mediate inflammatory responses to cytotoxic IgG antibodies or IgG immune complexes, despite the presence of a normal complement system. These results lead to the surprising conclusion that these two systems have evolved distinct functions in host immunity, with complement and its receptors mediating the interaction of natural antibodies (IgM) with pathogens to effect protection, while FcRs couple the interaction of IgG antibodies to effector cells to trigger inflammatory sequelae. These results necessitate a fundamental revision of the role of these antibody-binding systems in the immune response.
ISSN:0732-0582
1545-3278
DOI:10.1146/annurev.immunol.16.1.421