Oxidative Stress and Treg and Th17 Dysfunction in Systemic Lupus Erythematosus.
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.
Department of Dermatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Ji
0000-0001-8659-4206
J
Yang
Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China; Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, China.
Xue
X
Yang
Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai 200040, China; Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, China.
Hejian
0000-0002-2306-9778
H
Zou
Department of Dermatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Ming
0000-0001-8360-7729
M
Li
D002454:Cell Differentiation; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics*; D018384:Oxidative Stress; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism*; D058504:Th17 Cells / Q000378:metabolism*