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10.1016/j.cell.2017.03.011 http://scihub22266oqcxt.onion/10.1016/j.cell.2017.03.011 C5405738!5405738!28366204     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2017 ; 169 (2): 301-313.e11 Nephropedia Template TP {{tp|p=28366204|t=2017. RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation |pdf=|usr=}}{{28366204}} gab.com Text RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=28366204 #FOAvip Receptor-interacting kinase-3 (RIPK3) is an activator of necroptotic cell death, but recent work has implicated additional roles for RIPK3 in inflammatory signaling independent of cell death. However, while necroptosis has been shown to contribute to antiviral immunity, death-independent roles for RIPK3 in host defense have not been demonstrated. Using a mouse model of West Nile virus (WNV) encephalitis, we show that RIPK3 restricts WNV pathogenesis independently of cell death. Ripk3?/? mice exhibited enhanced mortality compared to WT controls, while mice lacking the necroptotic effector MLKL, or both MLKL and caspase-8, were unaffected. The enhanced susceptibility of Ripk3?/? mice arose from suppressed neuronal chemokine expression and decreased central nervous system (CNS) recruitment of T lymphocytes and inflammatory myeloid cells, while peripheral immunity remained intact. These data identify pleiotropic functions for RIPK3 in the restriction of viral pathogenesis, and implicate RIPK3 as a key coordinator of immune responses within the CNS. Twit Text FOAVip RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=28366204 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28366204 #FOAvip English Wikipedia <ref>{{Cite pmid|28366204}}</ref> RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation #MMPMID28366204 Daniels BP; Snyder AG; Olsen TM; Orozco S; Oguin TH; Tait SW; Martinez J; Gale M; Loo YM; Oberst A Cell 2017[Apr]; 169 (2): 301-313.e11 PMID28366204show ga Receptor-interacting kinase-3 (RIPK3) is an activator of necroptotic cell death, but recent work has implicated additional roles for RIPK3 in inflammatory signaling independent of cell death. However, while necroptosis has been shown to contribute to antiviral immunity, death-independent roles for RIPK3 in host defense have not been demonstrated. Using a mouse model of West Nile virus (WNV) encephalitis, we show that RIPK3 restricts WNV pathogenesis independently of cell death. Ripk3?/? mice exhibited enhanced mortality compared to WT controls, while mice lacking the necroptotic effector MLKL, or both MLKL and caspase-8, were unaffected. The enhanced susceptibility of Ripk3?/? mice arose from suppressed neuronal chemokine expression and decreased central nervous system (CNS) recruitment of T lymphocytes and inflammatory myeloid cells, while peripheral immunity remained intact. These data identify pleiotropic functions for RIPK3 in the restriction of viral pathogenesis, and implicate RIPK3 as a key coordinator of immune responses within the CNS. äRIPK3 restricts viral pathogenesis via cell death-independent neuroinf(epmc).pdf DeepDyve Pubget Overpricing