期刊
TRENDS IN IMMUNOLOGY
卷 42, 期 12, 页码 1054-1056出版社
CELL PRESS
DOI: 10.1016/j.it.2021.10.010
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资金
- National Institutes of Health [R01 AI128901]
Erythrocytes from lupus patients that fail to switch metabolic pathways retain their mitochondria, becoming a novel source of IFN when phagocytosed by macrophages.
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 differenti-ation retain their mitochondria. These mitochondria-containing erythrocytes represent a novel source of IFN when phagocytosed by macrophages.
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