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. 2016 Dec;7(1):11.
doi: 10.1007/s13317-016-0083-0. Epub 2016 Aug 4.

Reactive oxygen species in organ-specific autoimmunity

Giulia Di Dalmazi  1   2 , Jason Hirshberg  3 , Daniel Lyle  3 , Joudeh B Freij  4 , Patrizio Caturegli  5   6
Affiliations

Reactive oxygen species in organ-specific autoimmunity

Giulia Di Dalmazi et al. Auto Immun Highlights. 2016 Dec.

Abstract

Reactive oxygen species (ROS) have been extensively studied in the induction of inflammation and tissue damage, especially as it relates to aging. In more recent years, ROS have been implicated in the pathogenesis of autoimmune diseases. Here, ROS accumulation leads to apoptosis and autoantigen structural changes that result in novel specificities. ROS have been implicated not only in the initiation of the autoimmune response but also in its amplification and spreading to novel epitopes, through the unmasking of cryptic determinants. This review will examine the contribution of ROS to the pathogenesis of four organ specific autoimmune diseases (Hashimoto thyroiditis, inflammatory bowel disease, multiple sclerosis, and vitiligo), and compare it to that of a better characterized systemic autoimmune disease (rheumatoid arthritis). It will also discuss tobacco smoking as an environmental factor endowed with both pro-oxidant and anti-oxidant properties, thus capable of differentially modulating the autoimmune response.

Keywords: Autoimmunity; Hashimoto thyroiditis; Monoamine oxidase (MAO); Oxidative stress; Reactive oxygen species (ROS); Smoking.

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Conflict of interest statement

Giulia Di Dalmazi, Jason Hirshberg, Daniel Lyle, Joudeh B. Freij, and Patrizio Caturegli declare that they have no conflict of interest. Human and animal rights This article does not contain any studies with human participants or animals performed by any of the authors. Informed consent This is a review article and therefore, Informed Consent from patients is not necessary.

Figures

Fig. 1
Fig. 1
Schematic representation of the three major reactive oxygen species (superoxide, hydrogen peroxide, and hydroxyradical) and the enzymatic pathways that produce them. NADH nicotinamide adenine dinucleotide, NADPH nicotinamide adenine dinucleotide phosphate, GSH glutathione, GSSG glutathione disulfide, SOD superoxide dismutase, NOS nitric oxide synthases, MAO monoamine oxidase, MPO myeloperoxidase
Fig. 2
Fig. 2
Representation of the main cellular locations where ROS are produced. The abbreviations are the same as those used in Fig. 1, plus the following: Nox non-phagocytic NADPH oxidase, AQP aquaporin, GPx glutathione peroxidase, GR glutathione reductase, mPTP mitochondrial permeability transition pore, FAD flavin adenine dinucleotide, FADH2 flavin adenine dinucleotide
See this image and copyright information in PMC

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