Transcriptional Regulators and Modulate Inflammatory Response Genes in -infected Human Macrophages

Importance: Tuberculosis (TB) is one of the most serious infectious diseases, with high morbidity and mortality worldwide. C3HeB/FeJ mice are widely utilized for evaluating anti-TB drugs because their drug sensitivity and pathology during infection resemble those of human TB, including the development of necrotizing granulomas. Downregulation of the transcriptional regulatory genes and in C3HeB/FeJ mice has been demonstrated to activate gene expression associated with inflammatory responses during infection, resulting in susceptibility to the infection. Here, we examined the regulatory manner of and using transcriptomic analysis in -infected human macrophages. Depletion of and/or in -infected THP-1 macrophages impaired the induction of gene expression associated with inflammatory responses, including interferon response genes, compared with that in control macrophages. These results suggest that human and act as positive regulators for genes associated with inflammatory responses upon infection.