RANKL Induces IL-18 Binding Protein Expression in RAW264.7 Cells

• Takahashi Yumi

  Nihon University Graduate School of Dentistry

• Tanaka Hideki

  Department of Oral Health Sciences, Nihon University School of Dentistry Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry

• Nakai Kumiko

  Department of Oral Health Sciences, Nihon University School of Dentistry Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry

• Kitami Satoshi

  Department of Oral Health Sciences, Nihon University School of Dentistry

• Murakami Fumiko

  Nihon University Graduate School of Dentistry

• Morita Toyoko

  Department of Oral Health Sciences, Nihon University School of Dentistry The Lion Foundation for Dental Health

• Tanabe Natsuko

  Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry Department of Biochemistry, Nihon University School of Dentistry

• Kawato Takayuki

  Department of Oral Health Sciences, Nihon University School of Dentistry Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry

• Maeno Masao

  Department of Oral Health Sciences, Nihon University School of Dentistry Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry

抄録

The receptor activator of NF-κB (RANK) ligand (RANKL) is a cytokine that is essential for osteoclast development, whereas interleukin (IL)-18 suppresses osteoclastogenesis by increasing granulocyte-macrophage colony-stimulating factor (GM-CSF) production in T-cells. In the present study, we examined the effect of RANKL on the expression of IL-18 and IL-18 binding protein (IL-18BP), a natural inhibitor of IL-18, in RAW264.7 cells. We also examined the effect of conditioned medium derived from RAW264.7 cells on IL-18-induced GM-CSF expression in CD4⁺ T cells isolated from the spleens of C57BL/6J mice. mRNA expression of IL-18 was significantly suppressed, whereas that of IL-18BP was significantly increased in RANKL-treated RAW264.7 cells compared with untreated cells. RANKL also increased the expression of IL-18BP protein in culture supernatants of RAW264.7 cells. GM-CSF protein expression in CD4⁺ T-cells stimulated with IL-18 was suppressed by the addition of conditioned medium derived from RANKL-treated RAW264.7 cells. These results suggest that RANKL suppresses the stimulatory effect of IL-18 on GM-CSF expression in CD4⁺ T-cells via enhancing the production of IL-18BP in RAW264.7 cells.

収録刊行物

• Journal of Hard Tissue Biology

  Journal of Hard Tissue Biology 25 (2), 173-180, 2016

  硬組織再生生物学会

キーワード

• GM-CSF
• IL-18
• IL-18 binding protein
• RANKL

詳細情報

• CRID: 1390282679435715200
• NII論文ID: 130005145114
• NII書誌ID: AA11074332
• DOI: 10.2485/jhtb.25.173
• ISSN: 1880828X
• ISSN: 13417649
• NDL書誌ID: 027250754
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027250754
• Web Site: https://www.jstage.jst.go.jp/article/jhtb/25/2/25_173/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2016316637
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可