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Abstract
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.
Acknowledgements
Special thanks go to Gary Gilkeson, MD, for reviewing the manuscript before submission.
Declaration of interest: This publication was made possible by Grant AR045476 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, GCRC Grant M01RR001070, an award from the VA Research Enhancement Award Program, a VA Merit Award funding from the Arthritis Foundation, and the Alliance for Lupus Research. Special thanks go to Gary Gilkeson, MD, for reviewing the manuscript before submission. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.