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. 2021 Jun 19;69(4):312–322. doi: 10.1007/s12026-021-09203-6

Fig. 1.

Fig. 1

Schematic representation of TLR3 pathway. Poly-IC stimulates TLR3 which generates TRIF-dependent response by the conscription of TRIF to the cytoplasmic domain which then allows binding of TRIF to RIP1, TRAF6, TBK1 and TRAF3 resulting in activation of MAP kinases and IKK complex. MKK1/2, MKK3/6, and MKK4/7 activate ERK, JNK and p38, respectively and IκBα degradation releases NF-κ B. TBK1 phosphorylates IRF3 and 7. Nuclear translocation of NERK, JNK and p38 occurs which activates the transcription factor AP-1, and NF-κ B, IRF-3 and IRF-7 translocate to the nucleus. AP-1 and NF-κ B bind to the promoter regions of cytokine genes while IRF-3 and IRF-7 including NF-κB bind to the promoter region of chemokine genes and induce their transcription