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Osteoimmunology and Bone Biology
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Department of Orthopaedic Surgery, University of California Davis Health, Sacramento, CA, USA
Department of Molecular and Cell Biology, School of Natural Sciences, University of California, Merced, CA, USA
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Osteoimmunology and Bone Biology

Abstract submission deadline
closed (30 June 2024)
Manuscript submission deadline
31 December 2024
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19219

Topic Information

Dear Colleagues,

Traditionally, osteoimmunology investigated the molecular mechanisms underlying bone destruction associated with inflammatory diseases and focused primarily on the role of osteoclasts in bone homeostasis. In recent years, it has become increasingly clear that other pathologic conditions and genetic deficiencies in immunomodulatory molecules also elicit skeletal phenotypes. The advent of OMIC approaches has also revealed that the immune and bone systems share many molecules, including cytokines, chemokines, transcription factors, and signaling molecules and that bone cells reciprocally regulate immune cells and hematopoiesis. Here, we invite the submission of new studies that explore the role of immune cells and immune-cell-derived factors that control, regulate, or influence the function of osteoblasts, osteoclasts, and osteocytes. Similarly, we seek studies where defects in molecules expressed primarily in skeletal cells, or alleles associated with skeletal phenotypes, reciprocally affect the development, persistence, or behavior of immune cells in the bone marrow, or systemically.

Dr. Gabriela Loots
Dr. Jennifer O. Manilay
Topic Editors

Keywords

  • osteoimmunology
  • bone marrow niche
  • hematopoiesis
  • high bone mass
  • low bone mass
  • osteoclast
  • osteoblast
  • osteocyte
  • cytokines
  • chemokines
  • immune modulation
  • osteoarthritis
  • osteitis

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biology
biology 		3.6 5.7 2012 16.1 Days CHF 2700 Submit
Biomedicines
biomedicines 		3.9 5.2 2013 15.3 Days CHF 2600 Submit
Biomolecules
biomolecules 		4.8 9.4 2011 16.3 Days CHF 2700 Submit
Cells
cells 		5.1 9.9 2012 17.5 Days CHF 2700 Submit
International Journal of Molecular Sciences
ijms 		4.9 8.1 2000 18.1 Days CHF 2900 Submit
Journal of Clinical Medicine
jcm 		3.0 5.7 2012 17.3 Days CHF 2600 Submit

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Published Papers (10 papers)

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Osteogenic CpG oligodeoxynucleotide, iSN40, inhibits osteoclastogenesis in a TLR9-dependent manner
Authors: Rena Ikeda; Chihaya Kimura; Yuma Nihashi; Koji Umezawa; Takeshi Shimosato; Tomohide Takaya
Affiliation: Department of Agricultural and Life Sciences, Faculty of Agriculture, Shinshu University, Nagano, Japan
Abstract: Introduction: We recently identified a CpG oligodeoxynucleotide (CpG-ODN), iSN40 (5’-GGA ACG ATC CTC AAG CTT-3'), that promotes osteoblast differentiation independent of Toll-like receptor 9 (TLR9). While CpG-ODNs are known to be recognized by TLR9 and inhibit osteoclastogenesis. This study investigated the anti-osteoclastogenic effect of iSN40. Materials and Methods: The murine monocyte/macrophage cell line RAW264.7 was treated with receptor activator of NF-κB ligand (RANKL) to induce osteoclast differentiation. The effects of iSN40 and its variants on osteoclast formation were quantified by tartrate-resistant acid phosphatase (TRAP) staining and quantitative real-time RT-PCR. The TLR9 dependency of iSN40 was investigated using a TLR9 inhibitor, dihydrochloride (E6446). Intracellular incorporation of iSN40 was visualized using fluorescent dye-conjugated iSN40. Results: iSN40 completely inhibited RANKL-induced differentiation into TRAP+ multinuclear osteoclasts by suppressing osteoclastogenic genes (Nfatc1, Ctsk, and Dcstamp) and inducing anti- or non-osteoclastogenic genes (Irf8, Adgre1, and Il1b). Treatment with E6446 or mutation in the CpG motif of iSN40 abolished the anti-osteoclastogenic effect of iSN40 by interfering with its intracellular localization. These results demonstrate that iSN40 is subcellularly internalized, recognized by TLR9 via its CpG motif, modulates RANKL-dependent osteoclastogenic gene expression, and ultimately inhibits osteoclast formation. Conclusion: iSN40, which exerts both osteogenic and anti-osteoclastogenic effects, may be a promising nucleic acid drug for osteoporosis.

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