The dual role of Reactive Oxygen Species in autoimmune and inflammatory diseases: evidence from preclinical models

Hoffmann M, Griffiths HR (2018)


Publication Type: Journal article

Publication year: 2018

Journal

Book Volume: 125

Pages Range: 62-71

DOI: 10.1016/j.freeradbiomed.2018.03.016

Abstract

Reactive oxygen species (ROS) are created in cells during oxidative phosphorylation by the respiratory chain in the mitochondria or by the family of NADPH oxidase (NOX) complexes. The first discovered and most studied of these complexes, NOX2, mediates the oxidative burst in phagocytes. ROS generated by NOX2 are dreadful weapons: while being essential to kill ingested pathogens they can also cause degenerative changes on tissue if production and release are not balanced by sufficient detoxification. In the last fifteen years evidence has been accumulating that ROS are also integral signaling molecules and are important for regulating autoimmunity and immune-mediated inflammatory diseases. It seems that an accurate redox balance is necessary to sustain an immune state that both prevents the development of overt autoimmunity (the bright side of ROS) and minimizes collateral tissue damage (the dark side of ROS). Herein, we review studies from rodent models of arthritis, lupus, and neurodegenerative diseases that show that low NOX2-derived ROS production is linked to disease and elaborate on the underlying cellular and molecular mechanisms and the translation of these results to disease in humans.

Authors with CRIS profile

Involved external institutions

How to cite

APA:

Hoffmann, M., & Griffiths, H.R. (2018). The dual role of Reactive Oxygen Species in autoimmune and inflammatory diseases: evidence from preclinical models. Free Radical Biology and Medicine, 125, 62-71. https://dx.doi.org/10.1016/j.freeradbiomed.2018.03.016

MLA:

Hoffmann, Markus, and Helen R. Griffiths. "The dual role of Reactive Oxygen Species in autoimmune and inflammatory diseases: evidence from preclinical models." Free Radical Biology and Medicine 125 (2018): 62-71.

BibTeX: Download