124. Bone and Immune Cell Interactions

  1. Clifford J. Rosen MD
  1. Brendan F. Boyce

Published Online: 19 JUL 2013

DOI: 10.1002/9781118453926.ch124

Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition

Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition

How to Cite

Boyce, B. F. (2013) Bone and Immune Cell Interactions, in Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Eighth Edition (ed C. J. Rosen), John Wiley & Sons, Inc., Ames, USA. doi: 10.1002/9781118453926.ch124

Publication History

  1. Published Online: 19 JUL 2013

ISBN Information

Print ISBN: 9781118453889

Online ISBN: 9781118453926

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Keywords:

  • bone cell interactions;
  • immune cell interactions;
  • immune responses;
  • lymphocytes;
  • nuclear factor-kappa B (NF-κB);
  • osteoclast;
  • osteomyelitis;
  • RANKL

Summary

This chapter reviews current understanding of how bone and immune cell interactions affect the skeleton. Receptor activator of nuclear factor-kappa B ligand (RANKL) interaction with RANK activates nuclear factor-kappa B (NF-κB), a family of transcription factors that has essential functions in osteoclast precursors (OCPs) for their differentiation into osteoclasts (OCs). Importantly, in the context of immune responses and bone, NF-κB also regulates the differentiation and activation of immune cells, including B and T cells, maintenance of immune responses, and the development of lymph nodes. In addition to RANKL expressed by various cell types during inflammatory processes, so-called co-stimulatory signaling can also directly induce osteoclast formation through immunoglobulin-like receptors, including triggering receptor expressed in myeloid cells-2 (TREM-2) and osteoclast-associated receptor (OSCAR). Acute and chronic bone infections (osteomyelitis) typically result in localized lytic lesions at affected sites where increased osteoclastogenesis is induced by a number of mechanisms.