期刊
AUTOIMMUNITY
卷 43, 期 1, 页码 56-63出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/08916930903374683
关键词
Nitric oxide; systemic lupus erythematosus; reactive oxygen species; free radicals; oxidative stress
类别
资金
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [AR045476]
- GCRC [M01RR001070]
- VA Research Enhancement
- Arthritis Foundation
- Alliance for Lupus Research
Systemic lupus erythematosus (SLE) is an autoimmune syndrome marked by autoantibody production. Innate immunity is essential to transform humoral autoimmunity into the clinical lupus phenotype. Nitric oxide (NO) is a membrane-permeable signaling molecule involved in a broad array of biologic processes through its ability to modify proteins, lipids, and DNA and alter their function and immunogenicity. The literature regarding mechanisms through which NO regulates inflammation and cell survival is filled with contradictory findings. However, the effects of NO on cellular processes depend on its concentration and its interaction with reactive oxygen. Understanding this interaction will be essential to determine mechanisms through which reactive intermediates induce cellular autoimmunity and contribute to a sustained innate immune response and organ damage in SLE.
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