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. 2018 May 7;215(5):1273–1285. doi: 10.1084/jem.20180325

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© 2018 Moreira-Teixeira et al.

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Figure 1. — Alternative pathways of type I IFN induction during M. tuberculosis infection. Recognition of mycobacterial products by a range of cell surface and cytosolic PRR, including TLR4, NOD2, and STING, activates the kinase TBK1 leading to phosphorylation (P) and dimerization of IRF3 or IRF5, which translocates into the nucleus and promotes transcription of type I IFN genes. Release of mycobacterial or mitochondrial DNA in the cytosol activates cGAS, which synthesizes cGAMP. Host-derived cGAMP and/or mycobacterial-derived c-di-AMP activates the STING pathway and the downstream TBK1–IRF3 signaling axis. Peptidoglycan fragments can be sensed by NOD2 in the cytosol, activating the TBK1–IRF5 signaling pathway. Detection of extracellular M. tuberculosis and/or its products by TLR4 triggers TRIF-TBK1-IRF3–dependent induction of type I IFN by certain strains. Mtb, M. tuberculosis; mtDNA, mitochondrial DNA; PGN, peptidoglycan.