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10.1128/mBio.00342-18 http://scihub22266oqcxt.onion/10.1128/mBio.00342-18 C5874908!5874908!29559569     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       mBio 2018 ; 9 (2): ä Nephropedia Template TP {{tp|p=29559569|t=2018. Interleukin-1? Signaling in Dendritic Cells Induces Antiviral Interferon Responses |pdf=|usr=}}{{29559569}} gab.com Text Interleukin-1 Signaling in Dendritic Cells Induces Antiviral Interferon Responses JO: mBio http://www.kidney.de/pget.php?&tw=1&pmid=29559569 #FOAvip Induction of interferon beta (IFN-?), IFN-stimulated genes (ISGs), and inflammatory responses is critical for control of viral infection. We recently identified an essential linkage of stimulation of the inflammatory cytokine interleukin-1? (IL-1?) and induction of ISGs that function as host restriction pathways against the emerging flavivirus West Nile virus (WNV) in vivo. Here we utilized ex vivo global transcriptome analysis of primary dendritic cells, known targets of WNV replication, to define gene signatures required for this IL-1?-driven antiviral response. Dendritic cells that were deficient in IL-1 receptor signaling showed dysregulation of cell-intrinsic defense genes and loss of viral control during WNV infection. Surprisingly, we found that in wild-type cells, IL-1? treatment, in the absence of infection, drove the transcription of IFN-? and ISGs at late times following treatment. Expression of these antiviral innate immune genes was dependent on the transcription factor IFN regulatory factor 3 (IRF3) and appears to reflect a general shift in IL-1? signaling from an early inflammatory response to a late IFN-mediated response. These data demonstrate that inflammatory and antiviral signals integrate to control viral infection in myeloid cells through a process of IL-1?-to-IRF3 signaling crosstalk. Strategies to exploit these cytokines in the activation of host defense programs should be investigated as novel therapeutic approaches against individual pathogens. Twit Text FOAVip Interleukin-1 Signaling in Dendritic Cells Induces Antiviral Interferon Responses ????mBio http://www.kidney.de/pget.php?&tw=1&pmid=29559569 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29559569 #FOAvip English Wikipedia <ref>{{Cite pmid|29559569}}</ref> Interleukin-1? Signaling in Dendritic Cells Induces Antiviral Interferon Responses #MMPMID29559569 Aarreberg LD; Wilkins C; Ramos HJ; Green R; Davis MA; Chow K; Gale M mBio 2018[Mar]; 9 (2): ä PMID29559569show ga Induction of interferon beta (IFN-?), IFN-stimulated genes (ISGs), and inflammatory responses is critical for control of viral infection. We recently identified an essential linkage of stimulation of the inflammatory cytokine interleukin-1? (IL-1?) and induction of ISGs that function as host restriction pathways against the emerging flavivirus West Nile virus (WNV) in vivo. Here we utilized ex vivo global transcriptome analysis of primary dendritic cells, known targets of WNV replication, to define gene signatures required for this IL-1?-driven antiviral response. Dendritic cells that were deficient in IL-1 receptor signaling showed dysregulation of cell-intrinsic defense genes and loss of viral control during WNV infection. Surprisingly, we found that in wild-type cells, IL-1? treatment, in the absence of infection, drove the transcription of IFN-? and ISGs at late times following treatment. Expression of these antiviral innate immune genes was dependent on the transcription factor IFN regulatory factor 3 (IRF3) and appears to reflect a general shift in IL-1? signaling from an early inflammatory response to a late IFN-mediated response. These data demonstrate that inflammatory and antiviral signals integrate to control viral infection in myeloid cells through a process of IL-1?-to-IRF3 signaling crosstalk. Strategies to exploit these cytokines in the activation of host defense programs should be investigated as novel therapeutic approaches against individual pathogens. äInterleukin-1? Signaling in Dendritic Cells Induces Antiviral Interfer(epmc).pdf DeepDyve Pubget Overpricing