Effect of IFN-? on gene expression of bone marrow-derived macrophages

Here, we report that IFN-? derived from CD8+ T cells promotes the transcription of ACOD1 in macrophages and the subsequent production of itaconate. To explore the molecular mechanism by which IFN-? induces ACOD1 in macrophages, we analysed the transcriptome of IFN-?-treated BMDMs by RNA-seq. Enrichment analysis of differentially expressed genes (DEGs) revealed that the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway was significantly enriched in IFN-?-treated BMDMs compared with the control group. Overall design: To identify the molecular mechanism by which IFN-? induces ACOD1 in macrophages, we performed RNA-seq on untreated BMDMs and IFN-?-stimulated BMDMs. We then performed gene expression profiling analysis using data obtained from RNA-seq of BMDMs untreated or treated with IFN-? for 3 h. Comparative gene expression profiling analysis of RNA-seq data for untreated BMDMs and IFN-?-stimulated BMDMs.