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. 2014 Jun 19;40(6):989–1001. doi: 10.1016/j.immuni.2014.04.019

Figure 6.

Figure 6

Ahr-Deficient Murine and Human Keratinocytes Show Exacerbated Response to Inflammatory Stimuli

(A) mRNA expression of proinflammatory mediators in Ahr+/− (white bars) and Ahr−/− (black bars) murine keratinocytes stimulated for 24 hr with conditioned medium nCM and iCM. Data are expressed as fold change over stimulation with iCM over nCM medium.

(B) mRNA expression of proinflammatory mediators in Ahr+/− (white bars) and Ahr−/− (black bars) murine keratinocytes stimulated for 24 hr with recombinant IL-1β (10 ng/ml). Data expressed as fold change over medium control.

(C) Il1r1 mRNA expression in unstimulated murine primary keratinocytes from Ahr+/− (white bars) and Ahr−/− (black bars) mice.

(D) mRNA expression of proinflammatory mediators in human primary keratinocytes, transiently transfected for 48 hr with a nontargeting control SiRNA (cSiRNA, white bars) or in which AhR was transiently silenced (AhR-SiRNA, black bars), and stimulated for further 24 hr with human recombinant IL-1β (10 ng/ml).

(E) mRNA expression of proinflammatory mediators in human keratinocytes HaCaT cell lines, stable transfected with an empty vector (EV-HaCaT, white bars), or in which AhR had been stable silenced (AhR-silenced HaCaT, black bars), and stimulated for 24 hr with human recombinant IL-1β. Data expressed as fold change over medium control.

Results from one representative experiment of two or three independent experiments are shown. Plots show mean ± SEM; n = 3–6 wells per group. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗∗p < 0.0001.