Life Science Seminar

▶ Subject : Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity in the absence of adapitve immuity in mice

▶ Speaker : Hye-Young Kim(Division of immunologr and Allergy,Children`s Hospital Boston)

▶ Date : 5:00PM/ July 4(Mon)/2011

▶ Place : Auditorium, Postech Biotech Center

*Abstract

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.

☎ Inquiry : Yoon-keun Kim (T. 279-2125)