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Dr. Chang, Ya-Jen

Research Fellow
  • 02-27899050 (Lab) (Room No: N527)
  • 02-27898594 (Fax)

  1. Allergy and asthma
  2. Innate immunity and mucosal immunology
  3. Immunopharmacology

Education and Positions:
  • Ph.D., Pharmacology, National Taiwan University; 

    Instructor in Pediatrics, Harvard Medical School; 

    Research Associate in Immunology, Boston Children's Hospital

Highlight Detail

Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity

Dr. Chang, Ya-Jen
Nature Immunology, May 29, 2011

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.