Synoviolin is not a pathogenic factor for auto-inflammatory diseases

Tatsuaki Matsumoto, Yuiko Sato, Tami Kobayashi, Eri Ito, Tomoya Soma, Atsushi Kimura, Kana Miyamoto, Shu Kobayashi, Kengo Harato, Morio Matsumoto, Masaya Nakamura, Yasuo Niki, Takeshi Miyamoto

Research output: Contribution to journalArticlepeer-review


Auto-inflammatory syndromes are rare diseases characterized by arthritis and joint destruction, symptoms similar to but distinct from rheumatoid arthritis (RA). Therapeutic targets have not been well characterized for auto-inflammatory syndromes, although the E3 ligase Synoviolin was previously shown to be a novel therapeutic target for RA. Here, we show that Synoviolin loss has little impact on a model of auto-inflammatory diseases. We previously established such a model, the hIL-1 cTg mouse, in which IL-1 signaling was constitutively activated, and animals exhibit symptoms recapitulating auto-inflammatory syndromes such as major joint dominant arthritis. Here, we crossed hIL-1 cTg with Synoviolin flox'd mice to yield hIL-1 cTg/Synoviolin cKO mice. Synoviolin gene expression was ablated in adult hIL-1 cTg/Synoviolin cKO mice by injection of pIpC to activate Mx1 promoter-driven Cre recombinase. However, symptoms seen in hIL-1 cTg mice such as arthritis and joint destruction were not alleviated by targeting Synoviolin, ruling out Synoviolin as a therapeutic target for auto-inflammatory disease. Our results indicate that although similar, RA and auto-inflammatory diseases are different diseases, and treatment strategies should differ accordingly.

Original languageEnglish
Pages (from-to)183-188
Number of pages6
JournalBiochemical and Biophysical Research Communications
Publication statusPublished - 2021 Jun 18


  • Arthritis
  • Auto-inflammatory syndromes
  • IL-1
  • Rheumatoid arthritis
  • Synoviolin

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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