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Regulates TLR-Dependent Gene Expression of IFN-, IFN-
, IL-28, and IL-291
Department of Microbiology, National Public Health Institute, Helsinki, Finland
Toll-like receptors (TLRs) mediate host cell activation by various microbial components. TLR2, TLR3, TLR4, TLR7, TLR8, and TLR9 are the receptors that have been associated with virus-induced immune response. We have previously reported that all these TLRs, except TLR9, are expressed at mRNA levels in human monocyte-derived macrophages. Here we have studied TLR2, TLR3, TLR4, and TLR7/8 ligand-induced IFN-
, IFN-
, IL-28, and IL-29 expression in human macrophages. IFN- pretreatment of macrophages was required for efficient TLR3 and TLR4 agonist-induced activation of IFN-, IFN-, IL-28, and IL-29 genes. TLR7/8 agonist weakly activated IFN-, IFN-, IL-28, and IL-29 genes, whereas TLR2 agonist was not able to activate these genes. IFN- enhanced TLR responsiveness in macrophages by up-regulating the expression of TLR3, TLR4, and TLR7. IFN- also enhanced the expression of TLR signaling molecules MyD88, TIR domain-containing adaptor inducing IFN-, I
B kinase-
, receptor interacting protein 1, and IFN regulatory factor 7. Furthermore, the activation of transcription factor IFN regulatory factor 3 by TLR3 and TLR4 agonists was dependent on IFN- pretreatment. In conclusion, our results suggest that IFN- sensitizes cells to microbial recognition by up-regulating the expression of several TLRs as well as adapter molecules and kinases involved in TLR signaling.
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