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. 2011 Apr 15;23(6):357–364. doi: 10.1093/intimm/dxr019

Fig. 4.

Fig. 4.

A TLR4-dependent MyD88-IRAK-TRAF6-NF-κB signaling pathway is required for LPS-induced TLR3 expression. (A) Human blood monocytes or THP1 cells were pre-treated with functional antibody of TLR4 (TLR4fAb) for 1 h and then stimulated with LPS for 6 h as assessed by performing real-time Q-PCR analysis. (B) LPS markedly induced TLR3 expression at the mRNA level in HEK293-TLR4 cells, but only weakly in HEK293-pcDNA cells and HEK293-TLR2 cells. (C) Over-expression of dominant-negative MyD88, IRAK-1 or TRAF6 reduced LPS-induced TLR3 expression at the mRNA level in THP1 cells. (D) MG-132, a proteasome inhibitor that can inhibit NF-κB translocation, reduced LPS-induced TLR3 expression at the mRNA level in THP1 cells. The cells were pre-treated with MG-132 (1 μm) for 2 h and then treated with LPS for 6 h as assessed by performing real-time Q-PCR analysis. (E) p65 knockdown using p65 siRNA inhibited LPS-induced TLR3 expression at the mRNA level. These results are representative of three separate experiments. *P < 0.05 compared with control; **P < 0.05 compared with only LPS-treated groups.