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Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.91 Figure 2 Role of the immuno–skeletal interface in physiological osteoclast formation Figure 2 | Role of the immuno–skeletal interface in physiological osteoclast formation. Under physiological conditions, B cells, regulated by co-stimulatory interactions with T cells, supplement levels of osteoprotegerin (OPG) in the bone marrow. OPG decoys receptor activator of NF-κB ligand (RANKL), derived from multiple sources, moderating osteoclast resorption and stabilizing bone remodelling. Certain T-cell subpopulations including regulatory T (Treg) cells further secrete cytotoxic T-lymphocyte protein 4 (CTLA4), which can bind to CD80/CD86 on osteoclast precursors, thereby promoting apoptosis and diminishing bone resorption. BMSC, bone marrow stromal cell; MSC, mesenchymal stem cell; RANK, receptor activator of NF-κB. Weitzmann, M. N. & Ofotokun, I. (2016) Physiological and pathophysiological bone turnover — role of the immune system Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.91