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. 2005 Jun;79(11):6741–6750. doi: 10.1128/JVI.79.11.6741-6750.2005

FIG. 4.

FIG. 4.

VLP, but not assembly-defective HPV16 L1, mutants activate NF-κB- and AP-1-dependent transcription via MyD88. (A) The influence of in vitro-assembled HPV16 L1 mutant preparations upon NF-κB- and AP-1-dependent transcription in the macrophage cell line RAW264.7. Fold increase in chemiluminescence intensity after stimulation compared to unstimulated cells is plotted. (B) Assessment of the mRNA level of MyD88 in RAW264.7 cells by RT-PCR after stable transfection with siRNA constructs targeting MyD88 mRNA. (C) MyD88 knockdown (KD) blunts the NF-κB-dependent transcriptional response to TLR ligands LPS and CpG as well as HPV16 VLP. Results from three experiments are shown.