摘要：SummaryMyc has emerged as a pivotal transcription factor for four metabolic pathways: aerobic glycolysis, glutaminolysis, polyamine synthesis, and HIF-1α/mTOR. Each of these pathways accelerates the utilization of sugar. The BCG vaccine, a derivative ofMycobacteria-bovis, has been shown to trigger a long-term correction of blood sugar levels to near normal in type 1 diabetics (T1D). Here we reveal the underlying mechanisms behind this beneficial microbe-host interaction. We show that baseline glucose transport is deficient in T1D monocytes but is improved by BCGin vitroandin vivo. We then show, using RNAseq in monocytes and CD4 T cells, that BCG treatment over 56 weeks in humans is associated with upregulation of Myc and activation of nearly two dozen Myc-target genes underlying the four metabolic pathways. This is the first documentation of BCG induction of Myc and its association with systemic blood sugar control in a chronic disease like diabetes.Graphical AbstractDisplay OmittedHighlights•T1D has insufficient aerobic glycolysis; this causes insufficient sugar utilization•BCG vaccine lowers blood sugar levels in T1D by augmenting aerobic glycolysis•BCG-induced shift to aerobic glycolysis is associated with Myc activation•Host-microbe BCG interactions through Myc activate sugar-regulating genes in T1DImmune System; Diabetology; Transcriptomics
