Abstract
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of autoantibodies with subsequent immune complex deposition resulting in inflammatory injury to target organs. Reactive intermediates and for the purpose of this chapter, specifically reactive nitrogen intermediates (RNI), are important mediators of the innate immune system, tissue damage, and organ/cellular function in health and in lupus. RNI are under tight physiologic control due to the potency of their biologic activities. In SLE, enhanced production of RNI and/or impaired regulation may contribute to a break in immune tolerance, increase tissue damage, and alter enzyme function. This chapter reviews the latest evidence from both animal and human studies on the role of reactive nitrogen intermediates in the pathogenesis of SLE.
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