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. 2016 Feb 19;7:148. doi: 10.3389/fmicb.2016.00148

Figure 3.

Figure 3

Regulation of NF-κB and type 1 IFN signaling pathways by bacterial effectors. Bacterial infection triggers receptor-dependent activation of the signaling pathways at the host cell membrane. Receptor activation triggers signaling protein phosphorylation, which in turn activates the nuclear factor-kappaB (NF-κB) pathways via activation of the IκB kinase (IKK) complex and up-regulate interferon-regulatory factor (IRF) family of transcription factors through MyD88-mediated signaling. E. coli K1 IbeA-binding proteins Vimentin and PTB-associated splicing factor (PSF) act in concert to activate NF-κB. NF-κB activation induced by S. pneumoniae depends on the host factors toll-like receptors 2 (TLR2) and 4 (TLR4), and their ligands lipoteichoic acid (LTA) and lipopolysaccharide transport (LPT) (pneumococcal cell wall compounds). The NF-κB activation induced by L. monocytogenes depends on the Nucleotide-binding oligomerization domain-containing protein 1 (Nod1) and internalin B (InlB) receptor. The two coordinated signaling pathways result in production of inflammatory factors (NF-κB) and IFN-β (type 1 IFN signaling).