Cytokine-mediated signals as targets for treatment of rheumatoid arthritis: A JAK inhibitor in vitro and in vivo

Yoshiya Tanaka, Kunihiro Yamaoka

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Multiple cytokines play a pivotal role in the pathogenesis of rheumatoid arthritis (RA). For this to happen, the appropriate intracellular signaling pathways must be activated via cytokine receptors on the cell surface. Among them, members of JAK family are essential for the signaling pathways of various cytokines and are implicated in the pathogenesis of RA. An orally available JAK3 inhibitor tofacitinib (CP-690, 550) is currently in clinical trials for RA with satisfactory effects and acceptable safety results. Our in vitro experiments have indicated that the inhibition effect could be mediated through the suppression of IL-17 and IFN-g production and proliferation of CD4+ T cells. Here, we document the in vitro, ex vivo and in vivo effects of a JAK inhibitor for the treatment of RA.

Original languageEnglish
Pages (from-to)439-444
Number of pages6
JournalInternational Journal of Clinical Rheumatology
Volume6
Issue number4
DOIs
Publication statusPublished - 2011 Aug 1

Keywords

  • IL-6
  • JAK
  • STAT
  • TNF
  • rheumatoid arthritis
  • signal
  • treatment

ASJC Scopus subject areas

  • Rheumatology

Fingerprint Dive into the research topics of 'Cytokine-mediated signals as targets for treatment of rheumatoid arthritis: A JAK inhibitor in vitro and in vivo'. Together they form a unique fingerprint.

Cite this