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T cells and their role in bone anabolic activity



DOI:10.1038/bonekey.2012.126

Previous studies from this group revealed the unexpected; that intermittent treatment with parathyroid hormone (iPTH) stimulates T cells to produce Wnt10b, a Wnt ligand that activates Wnt signaling in osteoblasts, which, in turn, stimulates osteogenesis. In this study, Bedi et al. investigated whether this interaction relied on direct activation of the parathyroid hormone-related protein receptor (PPR) in T cells, using mice in which the PPR in T cells was conditionally silenced.

T cells from control mice showed a 6-fold increase in Wnt10b mRNA, whereas T cells from PPRT cells−/− mice showed no increase. In vivo experiments also confirmed that Wnt10b signaling in T cells was required for anabolic activity. Wnt10b−/− mice injected daily with iPTH for one week showed no increase in bone mineral density (BMD) or trabecular bone volume (BV), in contrast with wild type mice given the same treatment, which all showed significant increases in both BMD and trabecular BV.

Editor's comment: This new study provides further evidence that the interaction between PTH and osteoblasts is at least partly mediated by T cells. Discovering that T cells are involved in anabolic activity is a huge surprise and is difficult to reconcile with the more established observation that most inflammatory disorders are characterized by decreased bone formation. Glucocorticoids as immunosuppressants also decrease bone formation; could this be a T cell-mediated effect?


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