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Osteoimmunology

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Osteoimmunology (όστέον, osteon from Greek, “bone”; immunitas from Latin, “immunity”; and λόγος, logos, from Greek “study”) is a field that emerged about 40 years ago that studies the interface between the skeletal system and the immune system,[1][2] comprising the “osteo-immune system”.[3][4] Osteoimmunology also studies the shared components and mechanisms between the two systems in vertebrates, including ligands, receptors, signaling molecules and transcription factors. Over the past decade, osteoimmunology has been investigated clinically for the treatment of bone metastases, rheumatoid arthritis (RA), osteoporosis, osteopetrosis, and periodontitis. Studies in osteoimmunology reveal relationships between molecular communication among blood cells and structural pathologies in the body.[5]

System similarities

The RANKL-RANK-OPG (osteoprotegerin) axis is an example of an important signaling system functioning both in bone[6] and immune cell communication. RANKL is expressed on osteoblasts and activated T cells, whereas RANK is expressed on osteoclasts, and dendritic cells (DCs), both of which can be derived from myeloid progenitor cells. Surface RANKL on osteoblasts as well as secreted RANKL provide necessary signals for osteoclast precursors to differentiate into osteoclasts. RANKL expression on activated T cells leads to DC activation through binding to RANK expressed on DCs. OPG, produced by DCs, is a soluble decoy receptor for RANKL that competitively inhibits RANKL binding to RANK.[7]

Crosstalk

The bone marrow cavity is important for the proper development of the immune system, and houses important stem cells for maintenance of the immune system. Within this space, as well as outside of it, cytokines produced by immune cells also have important effects on regulating bone homeostasis. Some important cytokines that are produced by the immune system, including RANKL, M-CSF, TNFa, ILs, and IFNs, affect the differentiation and activity of osteoclasts and bone resorption.[8] Such inflammatory osteoclastogenesis and osteoclast activation can be seen in ex vivo primary cultures of cells from the inflamed synovial fluid of patients with disease flare of the autoimmune disease rheumatoid arthritis.[9]

Clinical osteoimmunology

Clinical osteoimmunology is a field that studies a treatment or prevention of the bone related diseases caused by disorders of the immune system. Aberrant and/or prolonged activation of immune system leads to derangement of bone modeling and remodeling. Common diseases caused by disorder of osteoimmune system is osteoporosis and bone destruction accompanied by RA characterized by high infiltration of CD4+ T cells in rheumatoid joints, in which two mechanisms are involved: One is an indirect effect on osteoclastogenesis from rheumatoid synovial cells in joints since synovial cells have osteoclast precursors and osteoclast supporting cells, synovial macrophages are highly differentiated into osteoclasts with help of RANKL released from osteoclast supporting cells.[10][11] The second is an indirect effect on osteoclast differentiation and activity by the secretion of inflammatory cytokines such as IL-1, IL-6, TNFa, in synovium of RA, which increase RANKL signaling and finally bone destruction. A clinical approach to prevent bone related diseases caused by RA is OPG and RANKL treatment in arthritis.

See also

References

  1. ^ Arron JR, Choi Y (November 2000). "Bone versus immune system". Nature. 408 (6812): 535–536. doi:10.1038/35046196. PMID 11117729.
  2. ^ Walsh MC, Kim N, Kadono Y, et al. (2006). "Osteoimmunology: interplay between the immune system and bone metabolism". Annu. Rev. Immunol. 24: 33–63. doi:10.1146/annurev.immunol.24.021605.090646. PMID 16551243.
  3. ^ Lorenzo J, Horowitz M, Choi Y (June 2008). "Osteoimmunology: interactions of the bone and immune system". Endocr Rev. 29 (4): 403–440. doi:10.1210/er.2007-0038. PMC 2528852. PMID 18451259.
  4. ^ Lorenzo J, Choi Y (2005). "Osteoimmunology". Immunol. Rev. 208: 5–6. doi:10.1111/j.0105-2896.2005.00340.x. PMID 16313336.
  5. ^ McHugh K (2008). "Osteoimmunology in skeletal cell biology and disease". Autoimmunity. 41 (3): 181–182. doi:10.1080/08916930701694808. PMID 18365830.
  6. ^ Zaidi M (November 2000). "Skeletal remodeling in health and disease". Nature Medicine. 13 (7): 791–801. doi:10.1038/nm1593. PMID 17618270.
  7. ^ Theill LE, Boyle WJ, Penninger JM (2002). "RANK-L and RANK: T cells, bone loss, and mammalian evolution". Annu. Rev. Immunol. 20: 795–823. doi:10.1146/annurev.immunol.20.100301.064753. PMID 11861618.
  8. ^ McInnes IB, Schett G (2007). "Cytokines in the pathogenesis of rheumatoid arthritis". Nat. Rev. Immunol. 7 (6): 429–442. doi:10.1038/nri2094. PMID 17525752.
  9. ^ Greisen, Stinne R.; Einarsson, Halldór Bjarki; Hvid, Malene; Hauge, Ellen-Margrethe; Deleuran, Bent; Kragstrup, Tue Wenzel (September 2015). "Spontaneous generation of functional osteoclasts from synovial fluid mononuclear cells as a model of inflammatory osteoclastogenesis". APMIS. 123 (9): 779–786. doi:10.1111/apm.12416.
  10. ^ Takayanagi, H. Oda H, Yamamoto S, Kawaguchi H, Tanaka S, Nishikawa T (1997). "A new mechanism of bone destruction in rheumatoid arthritis: synovial fibroblasts induce osteoclastogenesis". Biochemical and Biophysical Research Communications. 240 (2): 279–286. doi:10.1006/bbrc.1997.7404. PMID 9388467.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Takayanagi, H (2007). "Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems". Nat. Rev. Immunol. 7 (3): 292–304. doi:10.1038/nri2062. PMID 17380158.
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