Cited by 414Bone Metabolism and DiseasesRheumatoid Arthritis Research and TherapiesImmune Response and Inflammation

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Mechanistic insight into osteoclast differentiation in osteoimmunology

Takayanagi, Hiroshi·2005·Journal of Molecular Medicine

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Abstract

Recently a close relationship between the immune and skeletal systems or the interdisciplinary field called osteoimmunology has attracted much attention due to the observations that bone destruction is caused by an abnormal activation of the immune system in rheumatoid arthritis, and that mice lacking immunomodulatory molecules often exhibit an unexpected bone phenotype. Osteoclasts are cells of monocyte/macrophage origin that degrade the bone matrix. They are among the key players in the control of bone metabolism in health and disease. Receptor activator of NF-kappaB ligand (RANKL), a tumor necrosis factor (TNF) family cytokine, induces the differentiation of osteoclasts in the presence of macrophage-colony stimulating factor. RANKL activates TRAF6, c-Fos, and calcium signaling pathways, all of which are indispensable for the induction and activation of nuclear factor of activated T cells (NFAT) c1, the master transcription factor for osteoclastogenesis. The autoamplification of NFATc1 gene results in the efficient induction of osteoclast-specific genes. An AP-1 transcription factor complex containing c-Fos plays a crucial role in these processes, although results in conditional knockout mice show that Jun family members have a redundant role. The immunoreceptor tyrosine-based activation motif (ITAM) is an important signaling component for a number of receptors in the immune system including T-cell, B-cell, NK-cell, and Fc receptors, but its contribution to the skeletal sys…

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Authors: Takayanagi, H.
Affiliations: Tokyo Medical and Dental University (JP)
Corresponding author: Takayanagi, Hiroshi
Venue: Journal of Molecular Medicine
Publisher: Springer Science and Business Media LLC
Published: 2005-01-26
Volume: 83
Issue: 3
Pages: 170-179
ISSN: 0946-2716 (ISSN-L)
1432-1440
DOI: 10.1007/s00109-004-0612-6
OpenAlex: W2124273389
Cited by: 413
References: 76
Citations by year: 2026: 3 · 2025: 11 · 2024: 4 · 2023: 8 · 2022: 5 · 2021: 11 · 2020: 14 · 2019: 10 · 2018: 13 · 2017: 17 · 2016: 16 · 2015: 24 · 2014: 24 · 2013: 18 · 2012: 26
FWCI: 3.42
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Molecular Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: Takeda Science Foundation
Mitsubishi Foundation
Japan Society for the Promotion of Science
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: osteoclastogenesis, osteoimmunology, RANKL, TRAF6, c-fos, NFATc1, AP-1, ITAM signaling, FcRγ, DAP12, osteoclast-associated receptor, traps, TLR2, TLR4, phospholipase C-gamma, calcium signaling
MeSH terms: Animals, Carrier Proteins, Cell Differentiation, Humans, Membrane Glycoproteins, Osteoclasts, Receptors, Immunologic, Transcription Factors, Signal Transduction, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B

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Mechanistic insight into osteoclast differentiation in osteoimmunology

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