Rheumatoid arthritis: The role of reactive oxygen species in disease development and therapeutic strategies

Research output: Contribution to journalReview article

Abstract

Autoimmune diseases such as rheumatoid arthritis (RA) are chronic diseases that cannot be prevented or cured. If the pathologic basis of such diseases would be known, it might be easier to develop new drugs interfering with critical pathways. Genetic analysis of animal models for autoimmune diseases can result in discovery of proteins and pathways that play a key function in pathogenesis, which may provide rationales for new therapeutic strategies. Currently, only the MHC class II is clearly associated with human RA and animal models for RA. However, recent data from rats and mice with a polymorphism in Ncf1, a member of the NADPH oxidase complex, indicate a role for oxidative burst in protection from arthritis. Oxidative burst-activating substances can treat and prevent arthritis in rats, as efficiently as clinically applied drugs, suggesting a novel pathway to a therapeutic target in human RA. Here, the authors discuss the role of oxygen radicals in regulating the immune system and autoimmune disease. It is proposed that reactive oxygen species set the threshold for T cell activation and thereby regulate chronic autoimmune inflammatory diseases like RA. In the light of this new hypothesis, new possibilities for preventive and therapeutic treatment of chronic inflammatory diseases are discussed.

Details

Authors
  • Kyra Gelderman
  • Malin Hultqvist
  • Lina Olsson
  • Kristin Bauer
  • Angela Pizzolla
  • Peter Olofsson
  • Rikard Holmdahl
Organisations
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Cell and Molecular Biology
Original languageEnglish
Pages (from-to)1541-1567
JournalAntioxidants & Redox Signaling
Volume9
Issue number10
Publication statusPublished - 2007
Publication categoryResearch
Peer-reviewedYes

Bibliographic note

The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)