IFN-alpha Enhances TLR3-Mediated Antiviral Cytokine Expression in Human Endothelial and Epithelial Cells by Up-Regulating TLR3 Expression. Export

@article{citeulike:159074, abstract = {TLRs play a critical role in early innate immune response to virus infection. TLR3 together with TLR7 and TLR8 constitute a powerful system to detect genetic material of RNA viruses. TLR3 has been shown to bind viral dsRNA whereas TLR7 and TLR8 are receptors for viral single-stranded RNA. In this report we show that TLR7 or TLR8 are not expressed in human epithelial A549 cells or in HUVECs. Accordingly, A549 cells and HUVECs were unresponsive to TLR7/8 ligand R848. TLR3 was expressed at a higher level in HUVECs than in A549 cells. The TLR3 ligand poly(I:C) up-regulated IFN-beta, IL-28, IL-29, STAT1, and TLR3 expression in HUVECs but not in A549 cells. An enhanced TLR3 expression by transfection or by IFN-alpha stimulation conferred poly(I:C) responsiveness in A549 cells. Similarly, IFN-alpha pretreatment strongly enhanced poly(I:C)-induced activation of IFN-beta, IL-28, and IL-29 genes also in HUVECs. In conclusion, our results suggest that IFN-alpha-induced up-regulation of TLR3 expression is involved in dsRNA activated antiviral response in human epithelial and endothelial cells.}, address = {Department of Microbiology, National Public Health Institute, Helsinki, Finland.}, author = {Tissari, J. and Sir\'{e}n, J. and Meri, S. and Julkunen, I. and Matikainen, S.}, citeulike-article-id = {159074}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/15778392}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=15778392}, day = {1}, issn = {0022-1767}, journal = {J Immunol}, keywords = {cells, cytokine, genetics}, month = {April}, number = {7}, pages = {4289--4294}, posted-at = {2005-04-12 13:05:44}, priority = {2}, title = {IFN-{alpha} Enhances TLR3-Mediated Antiviral Cytokine Expression in Human Endothelial and Epithelial Cells by Up-Regulating TLR3 Expression.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/15778392}, volume = {174}, year = {2005} }

TY - JOUR ID - citeulike:159074 L3 - citeulike-article-id:159074 N2 - TLRs play a critical role in early innate immune response to virus infection. TLR3 together with TLR7 and TLR8 constitute a powerful system to detect genetic material of RNA viruses. TLR3 has been shown to bind viral dsRNA whereas TLR7 and TLR8 are receptors for viral single-stranded RNA. In this report we show that TLR7 or TLR8 are not expressed in human epithelial A549 cells or in HUVECs. Accordingly, A549 cells and HUVECs were unresponsive to TLR7/8 ligand R848. TLR3 was expressed at a higher level in HUVECs than in A549 cells. The TLR3 ligand poly(I:C) up-regulated IFN-beta, IL-28, IL-29, STAT1, and TLR3 expression in HUVECs but not in A549 cells. An enhanced TLR3 expression by transfection or by IFN-alpha stimulation conferred poly(I:C) responsiveness in A549 cells. Similarly, IFN-alpha pretreatment strongly enhanced poly(I:C)-induced activation of IFN-beta, IL-28, and IL-29 genes also in HUVECs. In conclusion, our results suggest that IFN-alpha-induced up-regulation of TLR3 expression is involved in dsRNA activated antiviral response in human epithelial and endothelial cells. IS - 7 JF - J Immunol SN - 0022-1767 AD - Department of Microbiology, National Public Health Institute, Helsinki, Finland. EP - 4294 TI - IFN-{alpha} Enhances TLR3-Mediated Antiviral Cytokine Expression in Human Endothelial and Epithelial Cells by Up-Regulating TLR3 Expression. VL - 174 SP - 4289 KW - cells KW - cytokine KW - genetics AU - Tissari, J AU - Sirén, J AU - Meri, S AU - Julkunen, I AU - Matikainen, S PY - 2005/04/01/ UR - http://view.ncbi.nlm.nih.gov/pubmed/15778392 ER -