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10.1126/scitranslmed.aac4227 http://scihub22266oqcxt.onion/10.1126/scitranslmed.aac4227 C4926955!4926955 !26424569     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26424569 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Transl+Med 2015 ; 7 (307 ): 307ra154 Nephropedia Template TP {{tp|p=26424569 |t=2015. Human IFNAR2 deficiency: Lessons for antiviral immunity |pdf=|usr=}}{{26424569 }} gab.com Text Human IFNAR2 deficiency: Lessons for antiviral immunity JO: Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26424569 #FOAvip Type I interferon (IFN-?/?) is a fundamental antiviral defense mechanism. Mouse models have been pivotal to understanding the role of IFN-?/? in immunity, although validation of these findings in humans has been limited. We investigated a previously healthy child with fatal encephalitis after inoculation of the live attenuated measles, mumps, and rubella (MMR) vaccine. By targeted resequencing, we identified a homozygous mutation in the high-affinity IFN-?/? receptor (IFNAR2) in the proband, as well as a newborn sibling, that rendered cells unresponsive to IFN-?/?. Reconstitution of the proband's cells with wild-type IFNAR2 restored IFN-?/? responsiveness and control of IFN-attenuated viruses. Despite the severe outcome of systemic live vaccine challenge, the proband had previously shown no evidence of heightened susceptibility to respiratory viral pathogens. The phenotype of IFNAR2 deficiency, together with similar findings in STAT2-deficient patients, supports an essential but narrow role for IFN-?/? in human antiviral immunity. Twit Text FOAVip Human IFNAR2 deficiency: Lessons for antiviral immunity ????Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26424569 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26424569 #FOAvip English Wikipedia <ref>{{Cite pmid|26424569 }}</ref> Human IFNAR2 deficiency: Lessons for antiviral immunity #MMPMID26424569 Duncan CJ ; Mohamad SM ; Young DF ; Skelton AJ ; Leahy TR ; Munday DC ; Butler KM ; Morfopoulou S ; Brown JR ; Hubank M ; Connell J ; Gavin PJ ; McMahon C ; Dempsey E ; Lynch NE ; Jacques TS ; Valappil M ; Cant AJ ; Breuer J ; Engelhardt KR ; Randall RE ; Hambleton S Sci Transl Med 2015[Sep]; 7 (307 ): 307ra154 PMID26424569 show ga Type I interferon (IFN-?/?) is a fundamental antiviral defense mechanism. Mouse models have been pivotal to understanding the role of IFN-?/? in immunity, although validation of these findings in humans has been limited. We investigated a previously healthy child with fatal encephalitis after inoculation of the live attenuated measles, mumps, and rubella (MMR) vaccine. By targeted resequencing, we identified a homozygous mutation in the high-affinity IFN-?/? receptor (IFNAR2) in the proband, as well as a newborn sibling, that rendered cells unresponsive to IFN-?/?. Reconstitution of the proband's cells with wild-type IFNAR2 restored IFN-?/? responsiveness and control of IFN-attenuated viruses. Despite the severe outcome of systemic live vaccine challenge, the proband had previously shown no evidence of heightened susceptibility to respiratory viral pathogens. The phenotype of IFNAR2 deficiency, together with similar findings in STAT2-deficient patients, supports an essential but narrow role for IFN-?/? in human antiviral immunity. |*Immunity [MESH] |Fatal Outcome [MESH] |Genes, Recessive [MESH] |Genetic Complementation Test [MESH] |Humans [MESH] |Infant [MESH] |Interferons/metabolism [MESH] |Receptor, Interferon alpha-beta/*deficiency/metabolism [MESH]Human IFNAR2 deficiency: Lessons for antiviral immunity (epmc).pdf DeepDyve Pubget Overpricing