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Correspondence to: Shizuo Akira, Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Yamada-oka 3-1, Suita, Osaka 565-0871, Japan. Tel:81-6-6879-8303 Fax:81-6-6879-8305 E-mail:sakira{at}biken.osaka-u.ac.jp.
T1/ST2, an orphan receptor with homology with the interleukin (IL)-1 receptor family, is expressed constitutively and stably on the surface of T helper type 2 (Th2) cells, but not on Th1 cells. T1/ST2 is also expressed on mast cells, which are critical for Th2-mediated effector responses. To evaluate whether T1/ST2 is required for Th2 responses and mast cell function, we have generated T1/ST2-deficient (T1/ST2-/-) mice and examined the roles of T1/ST2. Naive CD4+ T cells isolated from T1/ST2-/- mice developed to Th2 cells in response to IL-4 in vitro. T1/ST2-/- mice showed normal Th2 responses after infection with the helminthic parasite Nippostrongylus brasiliensis as well as in the mouse model of allergen-induced airway inflammation. In addition, differentiation and function of bone marrowderived cultured mast cells were unaffected. These findings demonstrate that T1/ST2 does not play an essential role in development and function of Th2 cells and mast cells.
Key Words: gene targeting, interleukin 1 receptor family, mast cell, asthma, T helper cells types 1 and 2
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