Immunoglobulin G inhibits glucocorticoid-induced osteoporosis through occupation of FcγRI

Lijuan Jiang; Wenlin Qiu; Xuefei Wang; Xiaoru Duan; Xiaoxiao Han; Tong Yu; Shenghui Wen; Zhijun Luo; Ruizhi Feng; Yao Teng; Haifeng Yin; Christian M Hedrich; Guo-Min Deng

doi:10.1016/j.isci.2023.107749

Immunoglobulin G inhibits glucocorticoid-induced osteoporosis through occupation of FcγRI

iScience. 2023 Aug 26;26(10):107749. doi: 10.1016/j.isci.2023.107749. eCollection 2023 Oct 20.

Authors

Affiliations

¹ Department of Rheumatology and Immunology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
² Department of Pediatric Rheumatology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK.

Abstract

Glucocorticoid-induced osteoporosis (GIOP) is a severe and common complication of long-term usage of glucocorticoids (GCs) and lacks of efficient therapy. Here, we investigated the mechanism of anti-inflammation effect and osteoclastogenesis side effect of GCs and immunoglobulin G (IgG) treatment against GIOP. GCs inhibited SLE IgG-induced inflammation, while IgG inhibited GCs-induced osteoclastogenesis. FcγRI and glucocorticoid receptor (GR) were found directly interacted with each other. GCs and IgG could reduce the expression of FcγRI on macrophages. The deficiency of FcγRI affected osteoclastogenesis by GCs and systemic lupus erythematosus (SLE) IgG-induced inflammation. Also, IgG efficiently reduced GIOP in mice. These data showed that GCs could induce osteoporosis and inhibit IgG-induced inflammation through FcγRI while IgG efficiently suppressed osteoporosis induced by GCs through FcγRI. Hence, our findings may help in developing a feasible therapeutic strategy against osteoporosis, such as GIOP.

Keywords: Cell biology; Immunology; Molecular biology.