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J Bone Miner Metab
J Bone Miner Metab
Journal of Bone and Mineral Metabolism
0914-8779
1435-5604
Springer Nature Singapore Singapore

39251416
1547
10.1007/s00774-024-01547-x
Correction
Correction: Crosstalk between bone and the immune system
http://orcid.org/0000-0001-5855-5357
Okamoto Kazuo okamotok@staff.kanazawa-u.ac.jp

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1 https://ror.org/057zh3y96 grid.26999.3d 0000 0001 2169 1048 Department of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan
2 https://ror.org/02hwp6a56 grid.9707.9 0000 0001 2308 3329 Division of Immune Environment Dynamics, Cancer Research Institute, Kanazawa University, Kakuma-Machi, Kanazawa, 920-1192 Japan
6 9 2024
6 9 2024
2024
42 4 481482
© The Author(s) 2024
2024
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pmcCorrection: Journal of Bone and Mineral Metabolism 10.1007/s00774-024-01539-x

In this article the top of Fig. 2 is cut off; the Fig. 2 should have appeared as shown below.Fig. 2 Mechanism of bone destruction in RA. The intricate immune–bone interaction among lymphocytes, fibroblasts, osteoclasts and osteoblasts drives the bone destruction in RA. IL-17 produced by Th17 cells induces RANKL expression in synovial fibroblasts. Th17 cells induce the proinflammatory cytokines including TNF, IL-6 and IL-1, which further upregulate RANKL expression. Synovial fibroblasts in RA consist of two main types: inflammatory fibroblasts in the sublining layer and RANKL+ tissue-destructive fibroblasts in the lining layer. The polarization of tissue-destructive synovial fibroblasts is controlled by the transcriptional factor ETS1. The immunoglobulin immune complexes directly promote osteoclastogenesis. Desialylated immune complexes are particularly effective in this process, regulated by an IL-23–Th17 cell-dependent mechanism. TNF induces the production of Wnt inhibitors like DKK1 and sclerostin, suppressing bone formation

The original article has been corrected.

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