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. 2006 Oct 30;25(51):6844–6867. doi: 10.1038/sj.onc.1209941

Figure 2.

Figure 2

Summary of the signaling pathways that recognize virus infection. Virus replication results in the production of PAMPs such as single- and double-stranded RNA. Viral nucleic acids trigger multiple signaling cascades through Toll-like-receptor-dependent (TLR3, TLR7 and TLR9) and TLR-independent (RIG-I and Mda-5) pathways leading to kinase activation through TRAF family members. In pDCs, TLR7 or TLR9 engagement by ssRNA leads to direct activation of IRF-7 through MyD88/TRAF6/IRAK4/IRAK1 recruitment. TRIF and MyD88 are the adaptors linking TLRs to the TRAF proteins, whereas MAVS links RIG-1 and Mda-5 to TRAF3. TRAF-dependent induction of the kinases JNK, IKKα, IKKβ, IKKɛ, TBK-1 and IRAK-1 induce the binding of ATF2-cJun, NF-κB (p50-RelA), IRF-3 and IRF-7 to sequence-specific PRD located upstream of the IFNβ start site. Coordinated assembly of these factors forms the IFNβ enhanceosome, which is responsible for the transcriptional induction of this antiviral cytokine (modified from tenOever and Maniatis, 2006).