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

Gelderman, Kyra LU ; Hultqvist, Malin LU ; Olsson, Lina LU ; Bauer, Kristin LU ; Pizzolla, Angela LU ; Olofsson, Peter LU and Holmdahl, Rikard LU (2007) In Antioxidants & Redox Signaling 9(10). p.1541-1567
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Antioxidants & Redox Signaling
volume
9
issue
10
pages
1541 - 1567
publisher
Mary Ann Liebert, Inc.
external identifiers
  • wos:000249521600001
  • scopus:34648839997
  • pmid:17678439
ISSN
1557-7716
DOI
10.1089/ars.2007.1569
language
English
LU publication?
yes
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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)
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0e5dfc11-38d4-48ff-b13a-c320449df589 (old id 656751)
date added to LUP
2016-04-01 16:03:48
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2020-10-04 06:11:07
@article{0e5dfc11-38d4-48ff-b13a-c320449df589,
  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.},
  author       = {Gelderman, Kyra and Hultqvist, Malin and Olsson, Lina and Bauer, Kristin and Pizzolla, Angela and Olofsson, Peter and Holmdahl, Rikard},
  issn         = {1557-7716},
  language     = {eng},
  number       = {10},
  pages        = {1541--1567},
  publisher    = {Mary Ann Liebert, Inc.},
  series       = {Antioxidants & Redox Signaling},
  title        = {Rheumatoid arthritis: The role of reactive oxygen species in disease development and therapeutic strategies},
  url          = {http://dx.doi.org/10.1089/ars.2007.1569},
  doi          = {10.1089/ars.2007.1569},
  volume       = {9},
  year         = {2007},
}