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Interleukin-35 upregulates OPG and inhibits RANKL in mice with collagen-induced arthritis and fibroblast-like

Y Li1, D Li1, Y Li1

  • 1Department of Rheumatology and Immunology, The First Affiliated Hospital of China Medical University, 155 Nanjing North Street, Heping District, Shenyang, 110001, People's Republic of China.

Osteoporosis International : a Journal Established As Result of Cooperation Between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA
|November 18, 2015
PubMed
Abstract

Insights

Interleukin-35 (IL-35) reduces bone erosion in rheumatoid arthritis by decreasing RANKL and increasing OPG. This novel cytokine shows potential for treating rheumatoid arthritis (RA) and associated osteoporosis.

Area of Science:

  • Immunology
  • Rheumatology
  • Osteoimmunology

Background:

  • Rheumatoid arthritis (RA) is characterized by bone erosion and osteoporosis.
  • The role of the anti-inflammatory cytokine interleukin-35 (IL-35) in RA pathogenesis, particularly bone destruction, is not fully understood.
  • Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) are key regulators of bone metabolism.

Purpose of the Study:

  • To investigate the effect of IL-35 on bone destruction in a rat model of collagen-induced arthritis (CIA).
  • To examine the impact of IL-35 on OPG and RANKL expression in CIA and cultured fibroblast-like synoviocytes (FLS).

Main Methods:

  • Thirty DBA/1J mice were divided into control, CIA, and CIA + IL-35 groups.
  • Collagen-induced arthritis was induced, and IL-35 was administered intraperitoneally.
  • Expression of IL-17, RANKL, and OPG was analyzed using RT-PCR and Western blot in vivo and in vitro.

Main Results:

  • CIA mice showed increased IL-17 and RANKL expression and decreased OPG expression.
  • IL-35 treatment ameliorated arthritis symptoms, reducing IL-17 and RANKL while increasing OPG levels.
  • IL-35 dose-dependently inhibited RANKL and increased OPG expression in cultured FLS.

Conclusions:

  • IL-35 effectively inhibits RANKL and promotes OPG expression in the context of CIA.
  • IL-35 demonstrates therapeutic potential for managing bone destruction in rheumatoid arthritis.
  • Further research into IL-35 as a treatment for RA is warranted.
Keywords:
Interleukin-35OPGRANKLRheumatic arthritis

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