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

Here, we report that IFN-γ 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-γ induces ACOD1 in macrophages, we analysed the transcriptome of IFN-γ-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-γ-treated BMDMs compared with the control group. To identify the molecular mechanism by which IFN-γ induces ACOD1 in macrophages, we performed RNA-seq on untreated BMDMs and IFN-γ-stimulated BMDMs. We then performed gene expression profiling analysis using data obtained from RNA-seq of BMDMs untreated or treated with IFN-γ for 3 h. Comparative gene expression profiling analysis of RNA-seq data for untreated BMDMs and IFN-γ-stimulated BMDMs.