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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2003-8-1
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pubmed:abstractText |
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(H)2) cells, but its role in T(H)2-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(H)2 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(H)2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T(H)2-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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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/SOCS3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/SOCS5 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/STAT4 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Socs3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Socs5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Stat4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Suppressor of Cytokine Signaling...,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1078-8956
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pubmed:author |
pubmed-author:CacalanoNicholasN,
pubmed-author:FukuyamaSatoruS,
pubmed-author:HamanoShinjiroS,
pubmed-author:HayashiKatsuhikoK,
pubmed-author:HimenoKunisukeK,
pubmed-author:Inagaki-OharaKyokoK,
pubmed-author:InoueHiromasaH,
pubmed-author:JohnstonJames AJA,
pubmed-author:KomineOkiruO,
pubmed-author:KuboMasatoM,
pubmed-author:MatsumotoKoichiroK,
pubmed-author:NagataNaokoN,
pubmed-author:O'GarraAnneA,
pubmed-author:OshidaTadahiloT,
pubmed-author:SaitoHirohisaH,
pubmed-author:SekiYoh-ichiY,
pubmed-author:YoshimuraAkihikoA
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pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1047-54
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12847520-Animals,
pubmed-meshheading:12847520-Asthma,
pubmed-meshheading:12847520-Bronchial Hyperreactivity,
pubmed-meshheading:12847520-Bronchial Provocation Tests,
pubmed-meshheading:12847520-DNA-Binding Proteins,
pubmed-meshheading:12847520-Dermatitis, Atopic,
pubmed-meshheading:12847520-Humans,
pubmed-meshheading:12847520-Hypersensitivity,
pubmed-meshheading:12847520-Interleukin-12,
pubmed-meshheading:12847520-Mice,
pubmed-meshheading:12847520-Mice, Inbred C57BL,
pubmed-meshheading:12847520-Mice, Transgenic,
pubmed-meshheading:12847520-Proteins,
pubmed-meshheading:12847520-Repressor Proteins,
pubmed-meshheading:12847520-STAT4 Transcription Factor,
pubmed-meshheading:12847520-Signal Transduction,
pubmed-meshheading:12847520-Suppressor of Cytokine Signaling Proteins,
pubmed-meshheading:12847520-Th2 Cells,
pubmed-meshheading:12847520-Trans-Activators,
pubmed-meshheading:12847520-Transcription Factors
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pubmed:year |
2003
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pubmed:articleTitle |
SOCS-3 regulates onset and maintenance of T(H)2-mediated allergic responses.
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pubmed:affiliation |
Research Institute for Biological Sciences, Tokyo University of Science, 2669 Yamazaki, Noda City, Chiba 278-0022, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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