Allergology International (Sep 2016)

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

  • Jun-ichiro Kan,
  • Shintaro Mishima,
  • Jun-ichi Kashiwakura,
  • Tomomi Sasaki-Sakamoto,
  • Masayuki Seki,
  • Shu Saito,
  • Chisei Ra,
  • Yasuaki Tokuhashi,
  • Yoshimichi Okayama

DOI
https://doi.org/10.1016/j.alit.2016.04.007
Journal volume & issue
Vol. 65, no. S
pp. S11 – S16

Abstract

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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-α, 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.

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