Nitric oxide in interstitial nephritis and other autoimmune diseases.
Nitric oxide can be generated by macrophages, as well as many other cell types, through a cytokine inducible isoform of nitric oxide synthase. Historically the effector functions ascribed to iNOS-generated NO have been the control of intracellular organisms and tumor cell cytotoxicity. However, there is a growing appreciation that iNOS generated NO can additionally play an important role in immunoregulation. In this review, the authors outline the effects of iNOS inhibition or genetic deletion on the expression of several autoimmune diseases and discuss potential mechanisms underlying the immunosuppressive effects of NO.
Kelly
C J
CJ
San Diego Veterans Affairs Healthcare System, University of California, USA.
Gold
D P
DP
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology*; D016207:Cytokines / Q000502:physiology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000188:drug therapy; D006801:Humans; D007108:Immune Tolerance; D008213:Lymphocyte Activation; D009395:Nephritis, Interstitial / Q000188:drug therapy / Q000209:etiology*; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D011914:Rats, Inbred BN; D018121:Receptors, Cytokine / Q000502:physiology
D016207:Cytokines; D018121:Receptors, Cytokine; D009569:Nitric Oxide; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat