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• W2144081914 abstract "<h3>Objective</h3> Under both physiological and pathological conditions, bone volume is determined by the rate of bone formation by osteoblasts and bone resorption by osteoclasts. Excessive bone loss is a common complication of human IBD whose mechanisms are not yet completely understood. Despite the role of activated CD4⁺ T cells in inflammatory bone loss, the nature of the T cell subsets involved in this process <i>in vivo</i> remains unknown. The aim of the present study was to identify the CD4⁺ T cell subsets involved in the process of osteoclastogenesis <i>in vivo</i>, as well as their mechanism of action. <h3>Design</h3> CD4⁺ T cells were studied in IL10−/− mice and Rag1−/− mice adoptively transferred with naive CD4⁺CD45RB^high T cells, representing two well-characterised animal models of IBD and in patients with Crohn9s disease. They were phenotypically and functionally characterised by flow cytometric and gene expression analysis, as well as in <i>in vitro</i> cocultures with osteoclast precursors. <h3>Results</h3> In mice, we identified bone marrow (BM) CD4⁺ T cells producing interleukin (IL)-17 and tumour necrosis factor (TNF)-α as an osteoclastogenic T cell subset referred to as Th17 TNF-α⁺ cells. During chronic inflammation, these cells migrate to the BM where they survive in an IL-7-dependent manner and where they promote the recruitment of inflammatory monocytes, the main osteoclast progenitors. A population equivalent to the Th17 TNF-α⁺ cells was also detected in patients with Crohn9s disease. <h3>Conclusions</h3> Our results highlight the osteoclastogenic function of the Th17 TNF-α⁺ cells that contribute to bone loss <i>in vivo</i> in IBD." @default.
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• W2144081914 date "2014-10-08" @default.
• W2144081914 modified "2023-10-18" @default.
• W2144081914 title "Bone marrow Th17 TNFα cells induce osteoclast differentiation, and link bone destruction to IBD" @default.
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• W2144081914 doi "https://doi.org/10.1136/gutjnl-2014-306947" @default.
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