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Oxidative stress in the pathology and treatment of systemic lupus erythematosus
Open accessAbstract
Oxidative stress is increased in systemic lupus erythematosus (SLE), and it contributes to immune system dysregulation, abnormal activation and processing of cell-death signals, autoantibody production and fatal comorbidities. Mitochondrial dysfunction in T cells promotes the release of highly diffusible inflammatory lipid hydroperoxides, which spread oxidative stress to other intracellular organelles and through the bloodstream. Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE. In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine-protein kinase mTOR undergoes redox-dependent activation. In turn, reversal of glutathione depletion by application of its amino acid precursor, N-acetylcysteine, improves disease activity in lupus-prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research. Blocking mTOR activation in T cells could conceivably provide a well-tolerated and inexpensive alternative approach to B-cell blockade and traditional immunosuppressive treatments. Nevertheless, compartmentalized oxidative stress in self-reactive T cells, B cells and phagocytic cells might serve to limit autoimmunity and its inhibition could be detrimental. Antioxidant therapy might also be useful in ameliorating damage caused by other treatments. This Review thus seeks to critically evaluate the complexity of oxidative stress and its relevance to the pathogenesis and treatment of SLE.
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“In various cell types, metabolic aberrations induced by mitochondrial abnormalities are linked to self-reactive and inflammatory phenotypes in autoimmune conditions, including SLE and RA68,69”
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“These events can lead to the generation of neoantigens that could be recognized as exogenous threats by the adaptive immune system68”
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Metadata
- Authors
- Perl, A.
- Venue
- Nature Reviews Rheumatology
- Published
- 2013-10-08
- Volume
- 9
- Issue
- 11
- Pages
- 674-686
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- PMC
- PMC4046645
- OpenAlex
- W2078472057
- Cited by
- 358
- References
- 139
- Citations by year
- 2026: 18 · 2025: 44 · 2024: 36 · 2023: 18 · 2022: 28 · 2021: 32 · 2020: 36 · 2019: 27 · 2018: 25 · 2017: 19 · 2016: 33 · 2015: 28 · 2014: 14
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01AI048079, R01AI072648, AI 048, AI 072)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (U01AR076092)
- National Center for Complementary and Integrative Health (AT-004332, R01AT004332)
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- oxidative stress, systemic lupus erythematosus, mitochondrial dysfunction, T cells, lipid hydroperoxides, glutathione depletion, mTOR, N-acetylcysteine, antioxidant therapy, autoimmunity, autoantibody production, disease activity, organ damage, lupus-prone mice
- MeSH terms
- Animals, Antioxidants, Humans, Lupus Erythematosus, Systemic, Autoimmunity, Oxidative Stress
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