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10.1038/ni.2045 http://scihub22266oqcxt.onion/10.1038/ni.2045 C3417123!3417123!21623379     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol ä ; 12 (7): 631-8 Nephropedia Template TP {{tp|p=21623379|t=ä. Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity |pdf=|usr=}}{{21623379}} gab.com Text Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21623379 #FOAvip Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (TH2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)?IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called ?natural helper cells?. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13. Twit Text FOAVip Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21623379 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21623379 #FOAvip English Wikipedia <ref>{{Cite pmid|21623379}}</ref> Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity #MMPMID21623379 Chang YJ; Kim HY; Albacker LA; Baumgarth N; McKenzie ANJ; Smith DE; DeKruyff RH; Umetsu DT Nat Immunol ä[]; 12 (7): 631-8 PMID21623379show ga Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (TH2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)?IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called ?natural helper cells?. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13. äInnate lymphoid cells mediate influenza-induced airway hyper-reactivit(epmc).pdf DeepDyve Pubget Overpricing