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Published Erratum
. 2024 Jul;42(4):481-482.
doi: 10.1007/s00774-024-01547-x.

Correction: Crosstalk between bone and the immune system

Kazuo Okamoto  1   2
Affiliations
Published Erratum

Correction: Crosstalk between bone and the immune system

Kazuo Okamoto. J Bone Miner Metab. 2024 Jul.
No abstract available

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Figures

Fig. 2
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
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