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10.1038/ni.2045

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suck abstract from ncbi


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pmid21623379
      Nat+Immunol 2011 ; 12 (7 ): 631-8
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  • Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity #MMPMID21623379
  • Chang YJ ; Kim HY ; Albacker LA ; Baumgarth N ; McKenzie AN ; Smith DE ; Dekruyff RH ; Umetsu DT
  • Nat Immunol 2011[May]; 12 (7 ): 631-8 PMID21623379 show 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 (T(H)2) 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.
  • |*Adaptive Immunity [MESH]
  • |Animals [MESH]
  • |Asthma/immunology/physiopathology [MESH]
  • |Bronchial Hyperreactivity/*immunology [MESH]
  • |Carrier Proteins/immunology [MESH]
  • |Female [MESH]
  • |Immunity, Innate [MESH]
  • |Influenza A virus/immunology [MESH]
  • |Interleukin-13/immunology [MESH]
  • |Interleukin-33 [MESH]
  • |Interleukins/immunology [MESH]
  • |Lymphocytes/*immunology [MESH]
  • |Macrophages, Alveolar/immunology [MESH]
  • |Mice [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |NLR Family, Pyrin Domain-Containing 3 Protein [MESH]
  • |Orthomyxoviridae Infections/*immunology [MESH]


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