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- W3037915028 endingPage "276" @default.
- W3037915028 startingPage "267" @default.
- W3037915028 abstract "The causes of systemic lupus erythematosus (SLE) are unknown; however, the pathogenesis is attributed, at least in part, to compartmentalized oxidative stress within the immune system. The accumulation of mitochondria is a prominent source of increased production of reactive oxygen intermediates (ROI) in T cells. In turn, ROI generate diffusible inflammatory lipid hydroperoxides, which spread oxidative stress to other intracellular organelles and through the bloodstream. ROI also emerge outside the immune system where they trigger auto-antigenicity of host proteins and organ damage. Depletion of the intracellular antioxidant, glutathione, leads to the activation of the mechanistic target of rapamycin (mTOR) that promotes pro-inflammatory lineage specification in T cells. The blockade of mTOR with N-acetylcysteine (NAC) or rapamycin shows therapeutic efficacy. Alternatively, deficient ROI production in phagocytic cells leads to the persistence of infectious organisms which may activate the innate immunity and enhance autoimmunity." @default.
- W3037915028 created "2020-07-02" @default.
- W3037915028 creator A5052080448 @default.
- W3037915028 date "2021-01-01" @default.
- W3037915028 modified "2023-09-25" @default.
- W3037915028 title "Metabolic control of lupus pathogenesis: central role for activation of the mechanistic target of rapamycin" @default.
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