Bone metabolism by immune complexes

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K15538
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Orthopaedic surgery
• Research Institution: Showa University
• Principal Investigator: Koga Takako 昭和大学, 歯学部, 講師 (90451905)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 破骨細胞 / RANKL / 免疫複合体 / 骨代謝 / 骨粗しょう症

Outline of Final Research Achievements

I investigated whether ICs regulate bone metabolism directly. Fcgr2b knockout mice lose bone upon the onset of a hypergammaglobulinemia or the administration of IgG1 ICs, which act mainly through FcgRIII. The IgG2 IC activates osteoclastogenesis by binding to FcgRI and FcgRIV, which is induced under inflammatory conditions. These results demonstrate a link between the adaptive immunity and bone, suggesting a regulatory role for ICs in bone resorption in general, and not only in inflammatory diseases.
In addition, I investigated the effects of an anti-RANKL antibody on maternal and newborn health in mice and found that anti-RANKL antibody administration during pregnancy results in not only an undesirable increase in bone mass, but also has harmful effects on newborn survival.

Free Research Field

骨免疫学