Interleukin-17A expression in human synovial mast cells in rheumatoid arthritis and osteoarthritis

  • Kan Jun-ichiro
    Allergy and Immunology Project Team, Nihon University School of Medicine Department of Orthopaedic Surgery, Nihon University School of Medicine
  • Mishima Shintaro
    Allergy and Immunology Project Team, Nihon University School of Medicine Department of Orthopaedic Surgery, Nihon University School of Medicine
  • Kashiwakura Jun-ichi
    Allergy and Immunology Project Team, Nihon University School of Medicine Laboratory for Allergic Disease, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI) Division of Medical Education Planning and Development, Nihon University School of Medicine
  • Sasaki-Sakamoto Tomomi
    Allergy and Immunology Project Team, Nihon University School of Medicine Division of Medical Education Planning and Development, Nihon University School of Medicine
  • Seki Masayuk
    Department of Orthopaedic Surgery, Nihon University School of Medicine
  • Saito Shu
    Department of Orthopaedic Surgery, Nihon University School of Medicine
  • Ra Chisei
    Department of Microbiology, Nihon University School of Medicine
  • Tokuhashi Yasuaki
    Department of Orthopaedic Surgery, Nihon University School of Medicine
  • Okayama Yoshimichi
    Allergy and Immunology Project Team, Nihon University School of Medicine Division of Medical Education Planning and Development, Nihon University School of Medicine

抄録

Background: Interleukin (IL)-17A plays a pivotal role in the pathogenesis of rheumatoid arthritis (RA). The expression of IL-17A in synovial mast cells (MCs) in RA and osteoarthritis (OA) has been reported, but the frequencies of IL-17A expression in synovial MCs have varied. The aim of this study was to investigate whether IL-17A expression is upregulated in human synovial MCs in RA and to elucidate the mechanism of IL-17A expression in synovial MCs. Methods: Synovial tissues were obtained from patients with RA or OA undergoing joint replacement surgery, and synovial MCs were enzymatically dispersed. Synovium-derived cultured MCs were generated by culturing synovial cells with stem cell factor. IL-17A expression was investigated using immunofluorescence in synovial tissues. IL-17A mRNA expression and its production from MCs were examined using RT-PCR and ELISA, respectively. Results: The number of IL-17A-positive (+) synovial MCs and the percentage of IL-17A+ MCs among all the IL-17A+ cells from RA patients were not significantly increased compared with those from OA subjects. The synovium-derived cultured MCs spontaneously released small amounts of IL-17A. Neither IgE- nor IgG-dependent stimulation increased IL-17A production from the MCs. IL-33, tumor necrosis factor-a, C5a, lipopolysaccharide or IL-23 plus IL-1β did not affect IL-17A production in MCs. Conclusions: The synovial MCs are not a main source of IL-17A in RA.

収録刊行物

  • Allergology International

    Allergology International 65 (Supplement.1), 11-16, 2016

    一般社団法人日本アレルギー学会

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