Annals of Translational Medicine · 2020 · 16 citations · 39 references
Life SciencesBiochemistryImmunologyAutoimmunityCell SignalingSignal TransductionGlycolysis RegulationImmune Cell MetabolismImmune Cell PhysiologyImmune Cell SignalingImmune PhysiologyMyasthenia GravisGlucose Metabolism BiomarkersGlucose Metabolism DisordersGlycolysis In Immune CellsImmune-metabolic InteractionImmunometabolic SignalingMyasthenia Gravis PharmacotherapyPeripheral Blood Immune Biomarkers
BACKGROUND: We investigated the correlation between glucose metabolism patterns of different immune cells and the metabolic regulatory signaling pathways in myasthenia gravis (MG) and aimed to identify therapeutic targets for MG. METHODS: experiments, we measured, the mRNA expression levels of mTOR, HIF-1α, B cell activating factor receptor (BAFF-R), GLUT1, HK, PFK, and PK, in addition to ECAR profiles, frequency of CD80 and CD86, and IgG levels from the culture supernatant of B cells (isolated from MG patients) treated with rapamycin and PX-478 (selective mTOR and HIF-1α inhibitor, respectively) from. RESULTS: , except IgG levels, the increased glycolysis levels, expression of key glycolytic enzymes, BAFF-R and frequency of CD80 and CD86 of B cells, could be inhibited by rapamycin and PX-478. CONCLUSIONS: Different subtypes of immune cells in MG exhibit different glucose metabolism patterns. The mTOR-HIF-1α signaling pathway might be the immunometabolism reprogramming checkpoint of glycolysis-dependent activated B cells in MG.
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