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. Author manuscript; available in PMC: 2009 Jun 18.
Published in final edited form as: Cell Host Microbe. 2008 Nov 13;4(5):470–483. doi: 10.1016/j.chom.2008.09.012

Figure 4. Increased Susceptibility of LEC-TLR4A/G to KSHV Infection.

Figure 4

(A) TLR4 expression in LEC-TLR4A/A (wild-type TLR4) and LEC-TLR4A/G (heterozygous mutation in TLR4 gene). Inserts show the corresponding pyrograms showing a 50% loss of the fourth peak (corresponding to A) and 50% increase of the third peak (corresponding to a G) in the mutant cells. Bar graph shows mRNA levels of TLR4 and TLR9 in LEC-TLR4A/A (gray bars) and LEC-TLR4A/G (black bars).

(B) mRNA levels of inflammatory cytokines and IFN-β in LEC-TLR4A/A (gray bars) and LEC-TLR4A/G (black bars) 6 hr poststimulation with LPS/sCD14. P values indicate significant changes compared to LEC-TLR4A/A. mRNA levels are corrected for background transcription (in nonstimulated LEC).

(C) Representative dot plot of KSHV infected LEC-TLR4A/A and LEC-TLR4A/G. Numbers correspond to percentage of infected cells.

(D) KSHV gene expression in KLEC-TLR4A/A (gray bars) and KLEC-TLR4A/G (black bars) 72 hr p.i. P values indicate significant changes compared to KLEC-TLR4A/A. In all panels, error bars represent standard deviation.