Mycobacterium tuberculosis inhibits type I interferon signaling to increase intracellular survival. Homo sapiens

Type I interferons (IFNα/β) are important for host defense against viral infections. In contrast, they are associated with exacerbated disease progression during infection with Mycobacterium tuberculosis. Here we report the surprising finding that M. tuberculosis inhibits IFN-receptor mediated cell signaling. The molecular mechanism of inhibition involves reduced phosphorylation of the transcription factors STAT1 and STAT2. We characterized the IFNβ transcriptome and the subset of genes that are deregulated upon M. tuberculosis infection of bone marrow-derived macrophages. This bioproject includes all the RNAseq data of the ex vivo infections.