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.
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15 November 1999
Brief Definitive Report|
November 15 1999
The Absence of Interleukin 1 Receptor–Related T1/St2 Does Not Affect T Helper Cell Type 2 Development and Its Effector Function
Katsuaki Hoshino,
Katsuaki Hoshino
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
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Shin-ichiro Kashiwamura,
Shin-ichiro Kashiwamura
cInstitute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Kozo Kuribayashi,
Kozo Kuribayashi
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Taku Kodama,
Taku Kodama
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Tohru Tsujimura,
Tohru Tsujimura
eDepartment of Pathology, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Kenji Nakanishi,
Kenji Nakanishi
cInstitute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Tomohiro Matsuyama,
Tomohiro Matsuyama
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
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Kiyoshi Takeda,
Kiyoshi Takeda
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
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Shizuo Akira
Shizuo Akira
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
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Katsuaki Hoshino
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
Shin-ichiro Kashiwamura
cInstitute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo 663-8501, Japan
Kozo Kuribayashi
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
Taku Kodama
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
Tohru Tsujimura
eDepartment of Pathology, Hyogo College of Medicine, Hyogo 663-8501, Japan
Kenji Nakanishi
cInstitute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo 663-8501, Japan
Tomohiro Matsuyama
dFifth Department of Internal Medicine, Hyogo College of Medicine, Hyogo 663-8501, Japan
Kiyoshi Takeda
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
Shizuo Akira
aDepartment of Host Defense, Research Institute for Microbial Diseases
bCore Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
Received:
September 09 1999
Accepted:
September 21 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 1999 The Rockefeller University Press
1999
The Rockefeller University Press
J Exp Med (1999) 190 (10): 1541–1548.
Article history
Received:
September 09 1999
Accepted:
September 21 1999
Citation
Katsuaki Hoshino, Shin-ichiro Kashiwamura, Kozo Kuribayashi, Taku Kodama, Tohru Tsujimura, Kenji Nakanishi, Tomohiro Matsuyama, Kiyoshi Takeda, Shizuo Akira; The Absence of Interleukin 1 Receptor–Related T1/St2 Does Not Affect T Helper Cell Type 2 Development and Its Effector Function. J Exp Med 15 November 1999; 190 (10): 1541–1548. doi: https://doi.org/10.1084/jem.190.10.1541
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