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. 2019 Apr 18;10:236. doi: 10.3389/fendo.2019.00236

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Copyright © 2019 Ponzetti and Rucci.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Regulation of immune cells by bone cells. Osteoclasts reduce hematopoietic stem cells (HSCs) homing by secreting cathepsin K (CTSK), which in turn degrades stromal cell-derived factor (SDF)1, stem cell factor (SCF), and osteopontin (OPN) depriving the bone niche of HSC-binding sites, which causes their mobilization. Osteoblasts, after stimulation with pro-osteoblastogenic factors such as intermittent parathyroid hormone (PTH), express Jagged1 (Jag1), which binds NOTCH1 on HSCs, and allows them to engraft and survive into the endosteal niche. B cells and bone cells communicate in multiple ways. For example, osteoblasts produce IL-7 and the chemokine CXCL12, that are fundamental for B-cells survival and activity.