Abstract
Type 1 interferon (IFN) is a major contributor to the pathogenesis of systemic lupus erythematosus (SLE). A landmark study by Caielli et al. now shows that erythrocytes from lupus patients that fail to switch from glycolysis to oxidative phosphorylation during differentiation retain their mitochondria. These mitochondria-containing erythrocytes represent a novel source of IFN when phagocytosed by macrophages.
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