IFN‐β modulates the response to TLR stimulation in human DC: Involvement of IFN regulatory factor‐1 (IRF‐1) in IL‐27 gene expression

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Abstract
Type I IFN are cytokines which play a central role in host resistance to viral or microbial infections and are important components linking innate and adaptive immunity. We and others have previously demonstrated that the production of IFN‐β by DC following bacterial infections or TLR triggering influences, in an autocrine manner, their maturation. In this study, we investigated whether IFN‐β release modulates the phenotype of the immature DC and their response to a subsequent TLR stimulation. The induction of CD86, HLA‐DR, CD38 and B7H1 and the absence of CCR7 and CD83 expression upon IFN‐β treatment suggest that IFN‐β‐primed DC remain at the site of infection acquiring an activated phenotype. These results prompted us to investigate the response of IFN‐β‐primed DC to TLR stimulation. While IFN‐β pretreatment increases slightly the expression of maturation markers in TLR2‐ or TLR4‐stimulated DC, it is able to modulate selectively the secretion of inflammatory and immuno‐regulating cytokines. Interestingly, IL‐27p28 subunit was induced by IFN‐β alone or during LPS‐induced maturation of DC in a type I IFN‐dependent manner through IFN regulatory factor‐1 (IRF‐1) activation. Taken together, our results shed light on the capacity of IFN‐β to finely tune DC response to invading pathogens.

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