Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2016, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2016/2526174
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Funding
- National Natural Science Foundation of China [81472874, 81401346, 81373213]
- Medical Guide Project from Shanghai Municipal Science and Technology [134119a8400]
- Cultivation Plan of Young Doctor of Shanghai
- Outstanding Talent Plan of Zhongshan Hospital, Fudan University [2015ZSYXGG13]
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Systemic lupus erythematosus (SLE) is an autoimmune disease that involves multiple organ systems. The pathogenic mechanisms that cause SLE remain unclear; however, it is well recognized that the immune balance is disturbed and that this imbalance contributes to the autoimmune symptoms of SLE. Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and the ability of the biological system to readily detoxify the reactive intermediates or to repair the resulting damage. In humans, oxidative stress is involved in many diseases, including atherosclerosis, myocardial infarction, and autoimmune diseases. Numerous studies have confirmed that oxidative stress plays an important role in the pathogenesis of SLE. This review mainly focuses on the recent research advances with respect to oxidative stress and regulatory T (Treg)/ helper T 17 (Th17) cell dysfunction in the pathogenesis of SLE.
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