SOCS-3 regulates onset and maintenance of TH2-mediated allergic responses

Yoh Ichi Seki; Hiromasa Inoue; Naoko Nagata; Katsuhiko Hayashi; Satoru Fukuyama; Koichiro Matsumoto; Okiru Komine; Shinjiro Hamano; Kunisuke Himeno; Kyoko Inagaki-Ohara; Nicholas Cacalano; Anne O'Garra; Tadahilo Oshida; Hirohisa Saito; James A. Johnston; Akihiko Yoshimura; Masato Kubo

doi:10.1038/nm896

SOCS-3 regulates onset and maintenance of T_H2-mediated allergic responses

Yoh Ichi Seki, Hiromasa Inoue, Naoko Nagata, Katsuhiko Hayashi, Satoru Fukuyama, Koichiro Matsumoto, Okiru Komine, Shinjiro Hamano, Kunisuke Himeno, Kyoko Inagaki-Ohara, Nicholas Cacalano, Anne O'Garra, Tadahilo Oshida, Hirohisa Saito, James A. Johnston, Akihiko Yoshimura, Masato Kubo

Department of Respirology

Research output: Contribution to journal › Article › peer-review

318 Citations (Scopus)

Abstract

Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (T_H2) cells, but its role in T _H2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased T_H2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased T_H2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T _H2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs.

Original language	English
Pages (from-to)	1047-1054
Number of pages	8
Journal	Nature medicine
Volume	9
Issue number	8
DOIs	https://doi.org/10.1038/nm896
Publication status	Published - Aug 1 2003

All Science Journal Classification (ASJC) codes

Biochemistry, Genetics and Molecular Biology(all)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/nm896

Cite this

Seki, Y. I., Inoue, H., Nagata, N., Hayashi, K., Fukuyama, S., Matsumoto, K., Komine, O., Hamano, S., Himeno, K., Inagaki-Ohara, K., Cacalano, N., O'Garra, A., Oshida, T., Saito, H., Johnston, J. A., Yoshimura, A., & Kubo, M. (2003). SOCS-3 regulates onset and maintenance of T_H2-mediated allergic responses. Nature medicine, 9(8), 1047-1054. https://doi.org/10.1038/nm896

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title = "SOCS-3 regulates onset and maintenance of TH2-mediated allergic responses",

abstract = "Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (TH2) cells, but its role in T H2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased TH2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased TH2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T H2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs.",

author = "Seki, {Yoh Ichi} and Hiromasa Inoue and Naoko Nagata and Katsuhiko Hayashi and Satoru Fukuyama and Koichiro Matsumoto and Okiru Komine and Shinjiro Hamano and Kunisuke Himeno and Kyoko Inagaki-Ohara and Nicholas Cacalano and Anne O'Garra and Tadahilo Oshida and Hirohisa Saito and Johnston, {James A.} and Akihiko Yoshimura and Masato Kubo",

note = "Funding Information: This work was supported by a Grant in Aid for Scientific Research on Priority Areas of the Ministry of Education, Culture, Sports, Science and Technology (Japan). Y.S. is a research fellow of the Japan Society for the Promotion of Science.",

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AU - Seki, Yoh Ichi

AU - Inoue, Hiromasa

AU - Nagata, Naoko

AU - Hayashi, Katsuhiko

AU - Fukuyama, Satoru

AU - Matsumoto, Koichiro

AU - Komine, Okiru

AU - Hamano, Shinjiro

AU - Himeno, Kunisuke

AU - Inagaki-Ohara, Kyoko

AU - Cacalano, Nicholas

AU - O'Garra, Anne

AU - Oshida, Tadahilo

AU - Saito, Hirohisa

AU - Johnston, James A.

AU - Yoshimura, Akihiko

AU - Kubo, Masato

N1 - Funding Information: This work was supported by a Grant in Aid for Scientific Research on Priority Areas of the Ministry of Education, Culture, Sports, Science and Technology (Japan). Y.S. is a research fellow of the Japan Society for the Promotion of Science.

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N2 - Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (TH2) cells, but its role in T H2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased TH2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased TH2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T H2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs.

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