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RIPK1 inhibition attenuates experimental autoimmune arthritis via suppression of osteoclastogenesis

Jooyeon Jhun1, Seung Hoon Lee1,2, Se-Young Kim1

  • 1The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.

Journal of Translational Medicine
|March 17, 2019
PubMed
Abstract

Insights

Necrostatin (NST)-1s, a necroptosis inhibitor, reduced collagen-induced arthritis (CIA) progression by decreasing inflammation and osteoclastogenesis. This suggests NST-1s may be a potential therapeutic for rheumatoid arthritis (RA).

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) is a systemic inflammatory disease marked by increased inflammatory cell death and osteoclastogenesis.
  • Necrostatin (NST)-1s inhibits receptor-interacting serine/threonine-protein kinase (RIPK)1, a key mediator of necroptosis.

Purpose of the Study:

  • To evaluate the efficacy of NST-1s in reducing inflammatory cell death and responses in a collagen-induced arthritis (CIA) mouse model.
  • To determine if NST-1s impacts osteoclastogenesis and T helper cell differentiation in CIA.

Main Methods:

  • Administration of NST-1s to mice with collagen-induced arthritis (CIA).
  • Assessment of disease progression, synovial expression of proinflammatory cytokines, and necroptosis mediators (RIPK1, RIPK3, MLKL).
  • In vitro and in vivo evaluation of osteoclastogenesis and T helper cell populations (Th1, Th17, Th2, Treg).

Main Results:

  • NST-1s treatment significantly decreased CIA progression and synovial expression of proinflammatory cytokines.
  • NST-1s reduced the expression of necroptosis mediators, including RIPK1, RIPK3, and MLKL.
  • The treatment inhibited osteoclastogenesis and modulated T helper cell profiles, favoring Th2 and Treg cells while downregulating Th1 and Th17 cells.

Conclusions:

  • NST-1s effectively attenuates collagen-induced arthritis (CIA) progression.
  • Inhibition of osteoclastogenesis and modulation of immune cell responses are key mechanisms of NST-1s action.
  • NST-1s shows potential as a therapeutic agent for rheumatoid arthritis (RA).
Keywords:
NecroptosisNecrostatin-1sOsteoclastogenesisRheumatoid arthritis

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