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Bone marrow Th17 TNFα cells induce osteoclast differentiation and link bone destruction to IBD
  1. Uta Syrbe,
  2. Britta Siegmund
  1. Department of Medicine (Gastroenterology, Infectious Diseases, Rheumatology), Charité–Universitätsmedizin Berlin, Berlin, Germany
  1. Correspondence to Dr Britta Siegmund, Department of Medicine (Gastroenterology, Infectious Diseases, Rheumatology), Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin 12200, Germany; britta.siegmund{at}

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Osteoporosis in IBD has long been attributed to impaired bone formation caused by malabsorption and consequent vitamin D and calcium deficiency or to long-term steroid therapy. However, systemic bone loss is not restricted to chronic inflammatory conditions of the intestine such as IBD or coeliac disease, but is also found in non-intestinal chronic inflammatory conditions including rheumatoid arthritis, ankylosing spondylitis and psoriatric arthritis.1 In a groundbreaking paper in 1999, rheumatologists started to shed light on the process of inflammation-induced bone loss.2 In this work by Kong and colleagues, the initial evidence indicated that T cells affect maturation of osteoclasts, the primary bone-resorbing cells. They showed in an arthritis model that systemically activated T cells are sufficient to induce receptor activator of NF-κB ligand (RANKL), which binds to its corresponding receptor RANK on osteoclast precursor cells, which ultimately induces their differentiation into osteoclasts. Hence, this work suggested a novel role for T cells in bone pathology. In the same year, the osteoclastogenic function of interleukin (IL)-17, at this time a newly discovered T-cell-derived cytokine, was first described. It was shown that IL-17 induces RANKL expression by osteoblasts, which further promotes osteoclast maturation. The presence of high levels of IL-17 in the synovial fluid of patients with rheumatoid arthritis led the authors to conclude that IL-17 is a crucial cytokine for osteoclastogenic bone resorption in …

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  • Competing interests None.

  • Provenance and peer review Commissioned; externally peer reviewed.

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