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. 2017 Jul 25;8(41):71249–71284. doi: 10.18632/oncotarget.19531

Figure 3. Signaling pathways of type I IFN inducers commonly used as adjuvants for cancer therapy.

Figure 3

Nearly all cells are capable of producing type I IFNs after sensing pathogen-associated microbial patterns (PAMPs) and danger-associated molecular patterns (DAMPs). This strategy is used to improve therapeutic cancer vaccines, increasing the immunologic response. The activation of pattern-recognition receptors (PRRs) leads to signaling through the adaptor molecules toll/interleukin-1 receptor domain-containing adaptor protein inducing interferon-β (TRIF) and/or Myd88, which culminates in the activation of IFN-regulatory factor 3/7 (IRF3/7) (yellow arrows) or nuclear factor-ĸB (NF-ĸB) (blue arrows) transcription factors and, consequently, in the expression of type I IFNs or inflammatory cytokines. Regarding the dendritic cell (DC) subtypes, the PRRs toll-like receptor (TLR)1, TLR2, TLR3, TLR4, TLR6 and TLR8 are expressed by monocyte-derived DCs and myeloid DCs, while TLR7 and TLR9 are only expressed by plasmacytoid DC. Lipopolysaccharide (LPS), triacylated lipopeptides (Pam3CSK4), diacylated lipopeptides (Pam2CSK4), polyribosinic-polyribocytidylic acid [Poly(I:C)], oligodeoxynucleotide (CpG ODN), TIR domain-containing adaptor protein (TIRAP), TRIF-related adaptor molecule (TRAM), 2′-3′-cyclic GMP-AMP (cGAMP), cGAMP synthase (cGAS), stimulator of interferon genes (STING).