期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 129, 期 10, 页码 4239-4244出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI127597
关键词
-
资金
- National Health and Medical Research Council (NHMRC) [APP1107001, APP1159901]
Macrophage activation in response to LPS is coupled to profound metabolic changes, typified by accumulation of the TCA cycle intermediates citrate, itaconate, and succinate. We have identified that endogenous type I IFN controls the cellular citrate/alpha-ketoglutarate ratio and inhibits expression and activity of isocitrate dehydrogenase (IDH); and, via C-13-labeling studies, demonstrated that autocrine type I IFN controls carbon flow through IDH in LPS-activated macrophages. We also found that type I IFN-driven IL-10 contributes to inhibition of IDH activity and itaconate synthesis in LPS-stimulated macrophages. Our findings have identified the autocrine type I IFN pathway as being responsible for the inhibition of IDH in LPS-stimulated macrophages.
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