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10.1038/gene.2014.22 http://scihub22266oqcxt.onion/10.1038/gene.2014.22 C4978536!4978536!24848930     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 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 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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Genes+Immun 2014 ; 15 (5): 320-32 Nephropedia Template TP {{tp|p=24848930|t=2014. An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following Influenza A H1N1 infection |pdf=|usr=}}{{24848930}} gab.com Text An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following Influenza A H1N1 infection JO: Genes Immun http://www.kidney.de/pget.php?&tw=1&pmid=24848930 #FOAvip Genetic and immunological analysis of host-pathogen interactions can reveal fundamental mechanisms of susceptibility and resistance to infection. Modeling human infectious diseases among inbred mouse strains is a proven approach but is limited by naturally occurring genetic diversity. Using ENU mutagenesis, we created a recessive loss-of-function point mutation in Unc93b1 (unc-93 homolog B1 (C. elegans)), a chaperone for endosomal TLR3, TLR7, and TLR9, that we termed Letr for ?loss of endosomal TLR response?. We used Unc93b1Letr/Letr mice to study the role of Unc93b1 in the immune response to influenza A/PR/8/34 (H1N1), an important global respiratory pathogen. During the early phase of infection, Unc93b1Letr/Letr mice had fewer activated exudate macrophages and decreased expression of CXCL10, IFN-?, and type I IFN. Mutation of Unc93b1 also led to reduced expression of the CD69 activation marker and a concomitant increase in the CD62L naïve marker on CD4+ and CD8+ T cells in infected lungs. Finally, loss of endosomal TLR signaling resulted in delayed viral clearance that coincided with increased tissue pathology during infection. Taken together, these findings establish a role for Unc93b1 and endosomal TLRs in the activation of both myeloid and lymphoid cells during the innate immune response to influenza. Twit Text FOAVip An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following Influenza A H1N1 infection ????Genes Immun http://www.kidney.de/pget.php?&tw=1&pmid=24848930 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24848930 #FOAvip English Wikipedia <ref>{{Cite pmid|24848930}}</ref> An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following Influenza A H1N1 infection #MMPMID24848930 Lafferty EI; Flaczyk A; Angers I; Homer R; d?Hennezel E; Malo D; Piccirillo CA; Vidal SM; Qureshi ST Genes Immun 2014[Jul]; 15 (5): 320-32 PMID24848930show ga Genetic and immunological analysis of host-pathogen interactions can reveal fundamental mechanisms of susceptibility and resistance to infection. Modeling human infectious diseases among inbred mouse strains is a proven approach but is limited by naturally occurring genetic diversity. Using ENU mutagenesis, we created a recessive loss-of-function point mutation in Unc93b1 (unc-93 homolog B1 (C. elegans)), a chaperone for endosomal TLR3, TLR7, and TLR9, that we termed Letr for ?loss of endosomal TLR response?. We used Unc93b1Letr/Letr mice to study the role of Unc93b1 in the immune response to influenza A/PR/8/34 (H1N1), an important global respiratory pathogen. During the early phase of infection, Unc93b1Letr/Letr mice had fewer activated exudate macrophages and decreased expression of CXCL10, IFN-?, and type I IFN. Mutation of Unc93b1 also led to reduced expression of the CD69 activation marker and a concomitant increase in the CD62L naïve marker on CD4+ and CD8+ T cells in infected lungs. Finally, loss of endosomal TLR signaling resulted in delayed viral clearance that coincided with increased tissue pathology during infection. Taken together, these findings establish a role for Unc93b1 and endosomal TLRs in the activation of both myeloid and lymphoid cells during the innate immune response to influenza. äAn ENU-induced splicing mutation reveals a role for Unc93b1 in early i(epmc).pdf DeepDyve Pubget Overpricing