Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 108K) PPT slides of all figures Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hoshino, K. Articles by Akira, S. Search for Related Content PubMed PubMed Citation Articles by Hoshino, K. Articles by Akira, S. Social Bookmarking                            What's this?

Brief Definitive Report

^a Department of Host Defense, Research Institute for Microbial Diseases
^b Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
^c Institute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo 663-8501, Japan
^d Fifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
^e Department of Pathology, Hyogo College of Medicine, Hyogo 663-8501, Japan
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Yamada-oka 3-1, Suita, Osaka 565-0871, Japan.81-6-6879-830581-6-6879-8303

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 marrow–derived 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

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Kurowska-Stolarska, M., Stolarski, B., Kewin, P., Murphy, G., Corrigan, C. J., Ying, S., Pitman, N., Mirchandani, A., Rana, B., van Rooijen, N., Shepherd, M., McSharry, C., McInnes, I. B., Xu, D., Liew, F. Y. (2009). IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation. J. Immunol. 183: 6469-6477 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS