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In this study, we characterized the dsRNA and dsDNA induced immune responses in human keratinocytes by studying pre- and posttranscriptional regulation of cytokine expression. • We compared the dsRNA and dsDNA induced cytokine expression in three keratinocyte cell types: NHEKs, HaCaT cells and HPV-KER cells. We found that transfection by the synthetic dsRNA and dsDNA analogue poly(I:C) and poly(dA:dT) induce the expression of IL-6 and TNF-α with notable kinetic differences and rate of induction. • We found that poly(I:C) and poly(dA:dT) induce the same inflammatory signaling pathways in keratinocytes, albeit with different kinetics and magnitude of activation. Our data revealed that transfection with poly(I:C) and poly(dA:dT) induced activation of NF-κB and STAT signaling, which along with p38 signaling were also shown to be functional in inducing cytokine mRNA expression. We also showed the negative regulatory role of ERK1/2 signaling in nucleotide-induced IL-6 mRNA expression in keratinocytes, which seems to be a celltype specific event. • By studying the expression pattern of PRINS lncRNA, we found decreased expression upon poly(dA:dT) transfection in NHEKs, while poly(I:C) did not led to altered expression of PRINS. • We have identified a potential negative regulatory role for PRINS lncRNA in poly(dA:dT) induced IL-6 and CCL-5 expression. In-depth analysis of this phenomenon revealed the sequence specific interaction between PRINS and the mRNA of IL-6 and CCL-5, which might be responsible for the posttranscriptional control of the mRNA expression. These results led us to hypothesize, that elevated PRINS expression in psoriatic uninvolved epidermis may contribute to downregulation of the inflammatory functions in psoriatic keratinocytes and maintenance of the normal phenotype.

Investigations on cytosolic nucleic acid fragment induced innate immune functions of keratinocytes