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Immune complexes regulate bone metabolism through FcRγ signalling
Takako Negishi-Koga1,2, Hans-Jürgen Gober3, Eriko Sumiya1
1Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.
Nature Communications
|April 1, 2015
Summary
Immune complexes (ICs) directly regulate bone resorption by influencing osteoclastogenesis. The balance of Fc gamma receptors (FcγRs) and ICs determines whether bone is lost or preserved in autoimmune conditions.
Area of Science:
- Immunology
- Bone Biology
- Rheumatology
Background:
- Autoantibody production and immune complex (IC) formation are common in autoimmune diseases linked to bone loss.
- The direct role of ICs in regulating bone metabolism remains poorly understood.
Purpose of the Study:
- To investigate whether immune complexes directly regulate bone metabolism.
- To elucidate the mechanisms by which ICs influence osteoclastogenesis and bone resorption.
Main Methods:
- Analysis of Fc gamma receptor (FcγR) expression and signaling pathways.
- Studies in Fcgr2b(-/-) mice, including induction of hypergammaglobulinemia and administration of IgG1 ICs.
- Investigation of IgG2 IC effects on osteoclastogenesis under inflammatory conditions.
Main Results:
- Osteoclastogenesis is regulated by the strength of FcRγ signaling, dependent on FcγR expression balance and IC availability.
- FcγRIII unexpectedly inhibits osteoclastogenesis under physiological conditions.
- IgG1 ICs induce bone loss via FcγRIII, while IgG2 ICs activate osteoclastogenesis through FcγRI and FcγRIV during inflammation.
Conclusions:
- Immune complexes play a direct regulatory role in bone resorption.
- A link exists between adaptive immunity and bone metabolism, extending beyond inflammatory diseases.
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