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10.4049/jimmunol.1701796 http://scihub22266oqcxt.onion/10.4049/jimmunol.1701796 C6089355!6089355!29848754     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2018 ; 201 (2): 573-82 Nephropedia Template TP {{tp|p=29848754|t=2018. IL-36? protects against severe influenza infection by promoting lung alveolar macrophage survival and limiting viral replication |pdf=|usr=}}{{29848754}} gab.com Text IL-36 protects against severe influenza infection by promoting lung alveolar macrophage survival and limiting viral replication JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29848754 #FOAvip While influenza virus infection remains a concerning disease for public health, the roles of individual cytokines during the immune response to influenza infection are not fully understood. We have identified IL-36? as a key mediator of immune protection during both high- and low-pathogenesis influenza infection. Il36g mRNA is upregulated in the lung following influenza infection and mice lacking IL-36? have greatly increased morbidity and mortality upon infection with either H1N1 or H3N2 influenza. The increased severity of influenza infection in IL-36?-deficient mice is associated with increased viral titers, higher levels of proinflammatory cytokines early in infection, and more diffuse pathology late in the disease course. Interestingly, the increased severity of disease in IL-36?-deficient mice correlates with a rapid loss of alveolar macrophages following infection. We find that the alveolar macrophages from naïve IL-36?-KO mice have higher expression of M2-like surface markers compared to WT mice, and show increased apoptosis within 24 hours of infection. Finally, transfer of WT alveolar macrophages to IL-36?-KO mice restores protection against lethal influenza challenge to levels observed in WT mice. Together, these data identify a critical role for IL-36? in immunity against influenza virus and demonstrate the importance of IL-36? signaling for alveolar macrophage survival during infection. Twit Text FOAVip IL-36 protects against severe influenza infection by promoting lung alveolar macrophage survival and limiting viral replication ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29848754 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29848754 #FOAvip English Wikipedia <ref>{{Cite pmid|29848754}}</ref> IL-36? protects against severe influenza infection by promoting lung alveolar macrophage survival and limiting viral replication #MMPMID29848754 Wein AN; Dunbar PR; McMaster SR; Tiger Li ZR; Denning TL; Kohlmeier JE J Immunol 2018[Jul]; 201 (2): 573-82 PMID29848754show ga While influenza virus infection remains a concerning disease for public health, the roles of individual cytokines during the immune response to influenza infection are not fully understood. We have identified IL-36? as a key mediator of immune protection during both high- and low-pathogenesis influenza infection. Il36g mRNA is upregulated in the lung following influenza infection and mice lacking IL-36? have greatly increased morbidity and mortality upon infection with either H1N1 or H3N2 influenza. The increased severity of influenza infection in IL-36?-deficient mice is associated with increased viral titers, higher levels of proinflammatory cytokines early in infection, and more diffuse pathology late in the disease course. Interestingly, the increased severity of disease in IL-36?-deficient mice correlates with a rapid loss of alveolar macrophages following infection. We find that the alveolar macrophages from naïve IL-36?-KO mice have higher expression of M2-like surface markers compared to WT mice, and show increased apoptosis within 24 hours of infection. Finally, transfer of WT alveolar macrophages to IL-36?-KO mice restores protection against lethal influenza challenge to levels observed in WT mice. Together, these data identify a critical role for IL-36? in immunity against influenza virus and demonstrate the importance of IL-36? signaling for alveolar macrophage survival during infection. äIL-36? protects against severe influenza infection by promoting lung a(epmc).pdf DeepDyve Pubget Overpricing