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RANKL biology: bone metabolism, the immune system, and beyond

Authors
  • Ono, Takehito1, 2
  • Hayashi, Mikihito1, 2
  • Sasaki, Fumiyuki1, 2
  • Nakashima, Tomoki1, 2
  • 1 Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan , Tokyo (Japan)
  • 2 Core Research for Evolutional Science and Technology (AMED-CREST), Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan , Tokyo (Japan)
Type
Published Article
Journal
Inflammation and Regeneration
Publisher
BioMed Central
Publication Date
Feb 07, 2020
Volume
40
Issue
1
Identifiers
DOI: 10.1186/s41232-019-0111-3
Source
Springer Nature
Keywords
License
Green

Abstract

Receptor activator of NF-κB (RANK) ligand (RANKL) induces the differentiation of monocyte/macrophage–lineage cells into the bone–resorbing cells called osteoclasts. Because abnormalities in RANKL, its signaling receptor RANK, or decoy receptor osteoprotegerin (OPG) lead to bone diseases such as osteopetrosis, the RANKL/RANK/OPG system is essential for bone resorption. RANKL was first discovered as a T cell-derived activator of dendritic cells (DCs) and has many functions in the immune system, including organogenesis, cellular development. The essentiality of RANKL in the bone and the immune systems lies at the root of the field of “osteoimmunology.” Furthermore, this cytokine functions beyond the domains of bone metabolism and the immune system, e.g., mammary gland and hair follicle formation, body temperature regulation, muscle metabolism, and tumor development. In this review, we will summarize the current understanding of the functions of the RANKL/RANK/OPG system in biological processes.

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