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Regulation of ILC2 activities in allergic inflammation September 22(Tue), 11:00 / Auditorium (1F), PBC Shigeo Koyasu RIKEN Center for Integrative Medical Sciences, Keio University School of Medicine The type 2 immune response, characterized by the production of IL-4, IL-5 and IL-13, is a critical immune response against helminths invading cutaneous or mucosal sites. In addition, type 2 immune responses are involved in the pathophysiology of various allergic diseases including asthma. Type 2 cytokines are induced soon after helminth infection or certain allergic responses such as papaininduced airway inflammation even before an antigen-specific adaptive immune response is established. We have identified a previously unidentified lymphocyte population producing large amounts of type 2 cytokines, which we named Natural helper (NH) cells and are now a member of group 2 innate lymphoid cells (ILC2s). We identified ILC2s in lymphoid clusters in adipose tissues, which we termed fat-associated lymphoid cluster (FALC). ILC2s produce type 2 cytokines constitutively without any stimulation, and support the self-renewal of B1 cells and IgA production by B cells. Stimulation by IL-33 or helminth infection activates ILC2s to produce large amounts of IL-5 and IL-13, which induce eosinophilia and goblet cell hyperplasia, both of which play an important role in anti-helminth immunity and pathophysiology of allergic diseases. We have recently found that IFNγ and IL-27 suppress tissueresident ILC2s that expand in situ without migration during helminth infection and fungi infection in a STAT1-dependent manner. ILC2-mediated lung inflammation was enhanced in the absence of IFNγ receptor signals in vivo. Our results suggest that IFNγ- and IL-27-mediated suppression of tissue-resident ILC2s is a negative feedback mechanism for ILC2 functions in vivo. Inquiry: AIM Administrative Team (Tel.279-8628, E-mail: [email protected])