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10.1002/hep.26981 http://scihub22266oqcxt.onion/10.1002/hep.26981 C4273749!4273749!24375615     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hepatology 2014 ; 60 (1): 237-49 Nephropedia Template TP {{tp|p=24375615|t=2014. Toll-like receptor 7-mediated Type I Interferon signaling prevents cholestasis- and hepatotoxin-induced liver fibrosis |pdf=|usr=}}{{24375615}} gab.com Text Toll-like receptor 7-mediated Type I Interferon signaling prevents cholestasis- and hepatotoxin-induced liver fibrosis JO: Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=24375615 #FOAvip Toll-like receptor 7 (TLR7) signaling predominantly regulates production of type I Interferons (IFNs), which has been suggested in clinical studies to be anti-fibrotic. However, the mechanistic role of the TLR7-type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver fibrosis was induced in wild-type (WT), TLR7-deficient, and IFN-?/? receptor-1 (IFNAR1)-deficient mice and TLR7-mediated signaling was assessed in liver cells isolated from these mice. TLR7-deficient and IFNAR1-deficient mice were more susceptible to liver fibrosis than WT mice, indicating that TLR7-type I IFN signaling exerts a protective effect against liver fibrosis. Notably, the hepatic expression of IL-1ra was suppressed in TLR7- or IFNAR1-deficient mice compared with respective WT mice, and treatment with recombinant IL-1ra reduced liver fibrosis. In vivo activation of TLR7 significantly increased IFNa4 and IL-1ra expression in the liver. Interestingly, each cytokine had different cellular source showing that dendritic cells (DCs) are responsible cell type for production of type I IFN, while Kupffer cells (KCs) mainly produce IL-1ra in response to type I IFN. Furthermore, TLR7 activation by R848 injection suppressed liver fibrosis and production of pro-inflammatory cytokines, and these effects were dependent on type I IFN signaling. Consistent with in vivo data, IFN? significantly induced IL-1ra production in primary KCs.Conclusions: TLR7 signaling activates DCs to produce type I IFN, which in turn induces anti-fibrogenic IL-1ra production in KCs. Thus, manipulation of the TLR7-type I IFN-IL-1ra axis may be a new therapeutic strategy for the treatment of liver fibrosis. Twit Text FOAVip Toll-like receptor 7-mediated Type I Interferon signaling prevents cholestasis- and hepatotoxin-induced liver fibrosis ????Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=24375615 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24375615 #FOAvip English Wikipedia <ref>{{Cite pmid|24375615}}</ref> Toll-like receptor 7-mediated Type I Interferon signaling prevents cholestasis- and hepatotoxin-induced liver fibrosis #MMPMID24375615 Roh YS; Park S; Kim JW; Lim CW; Seki E; Kim B Hepatology 2014[Jul]; 60 (1): 237-49 PMID24375615show ga Toll-like receptor 7 (TLR7) signaling predominantly regulates production of type I Interferons (IFNs), which has been suggested in clinical studies to be anti-fibrotic. However, the mechanistic role of the TLR7-type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver fibrosis was induced in wild-type (WT), TLR7-deficient, and IFN-?/? receptor-1 (IFNAR1)-deficient mice and TLR7-mediated signaling was assessed in liver cells isolated from these mice. TLR7-deficient and IFNAR1-deficient mice were more susceptible to liver fibrosis than WT mice, indicating that TLR7-type I IFN signaling exerts a protective effect against liver fibrosis. Notably, the hepatic expression of IL-1ra was suppressed in TLR7- or IFNAR1-deficient mice compared with respective WT mice, and treatment with recombinant IL-1ra reduced liver fibrosis. In vivo activation of TLR7 significantly increased IFNa4 and IL-1ra expression in the liver. Interestingly, each cytokine had different cellular source showing that dendritic cells (DCs) are responsible cell type for production of type I IFN, while Kupffer cells (KCs) mainly produce IL-1ra in response to type I IFN. Furthermore, TLR7 activation by R848 injection suppressed liver fibrosis and production of pro-inflammatory cytokines, and these effects were dependent on type I IFN signaling. Consistent with in vivo data, IFN? significantly induced IL-1ra production in primary KCs.Conclusions: TLR7 signaling activates DCs to produce type I IFN, which in turn induces anti-fibrogenic IL-1ra production in KCs. Thus, manipulation of the TLR7-type I IFN-IL-1ra axis may be a new therapeutic strategy for the treatment of liver fibrosis. äToll-like receptor 7-mediated Type I Interferon signaling prevents cho(epmc).pdf DeepDyve Pubget Overpricing