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rdf:type |
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lifeskim:mentions |
umls-concept:C0026809,
umls-concept:C0039194,
umls-concept:C0178539,
umls-concept:C0221099,
umls-concept:C0301625,
umls-concept:C0678227,
umls-concept:C0700624,
umls-concept:C0871261,
umls-concept:C1325847,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
3
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pubmed:dateCreated |
2002-9-30
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pubmed:abstractText |
Interleukin-17 (IL-17) is a proinflammatory cytokine produced by T cells. The involvement of IL-17 in human diseases has been suspected because of its detection in sera from asthmatic patients and synovial fluids from arthritic patients. In this study, we generated IL-17-deficient mice and investigated the role of IL-17 in various disease models. We found that contact, delayed-type, and airway hypersensitivity responses, as well as T-dependent antibody production, were significantly reduced in the mutant mice, while IL-17 deficiency of donor T cells did not affect acute graft-versus-host reaction. The results suggest that impaired responses were caused by the defects of allergen-specific T cell activation. Our findings indicate that IL-17 plays an important role in activating T cells in allergen-specific T cell-mediated immune responses.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1074-7613
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
375-87
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12354389-Acute Disease,
pubmed-meshheading:12354389-Animals,
pubmed-meshheading:12354389-Antibody Formation,
pubmed-meshheading:12354389-B-Lymphocytes,
pubmed-meshheading:12354389-Bronchial Hyperreactivity,
pubmed-meshheading:12354389-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12354389-Cells, Cultured,
pubmed-meshheading:12354389-Coculture Techniques,
pubmed-meshheading:12354389-Dendritic Cells,
pubmed-meshheading:12354389-Dermatitis, Allergic Contact,
pubmed-meshheading:12354389-Dinitrofluorobenzene,
pubmed-meshheading:12354389-Female,
pubmed-meshheading:12354389-Graft vs Host Reaction,
pubmed-meshheading:12354389-Haptens,
pubmed-meshheading:12354389-Hypersensitivity, Delayed,
pubmed-meshheading:12354389-Immunity, Cellular,
pubmed-meshheading:12354389-Interleukin-17,
pubmed-meshheading:12354389-Lymphocyte Activation,
pubmed-meshheading:12354389-Lymphocyte Cooperation,
pubmed-meshheading:12354389-Male,
pubmed-meshheading:12354389-Mice,
pubmed-meshheading:12354389-Mice, Inbred BALB C,
pubmed-meshheading:12354389-Mice, Inbred C57BL,
pubmed-meshheading:12354389-Mice, Knockout,
pubmed-meshheading:12354389-Mitogens,
pubmed-meshheading:12354389-Models, Animal,
pubmed-meshheading:12354389-Nickel,
pubmed-meshheading:12354389-Picryl Chloride,
pubmed-meshheading:12354389-Specific Pathogen-Free Organisms,
pubmed-meshheading:12354389-Spleen,
pubmed-meshheading:12354389-T-Lymphocyte Subsets,
pubmed-meshheading:12354389-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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pubmed:articleTitle |
Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses.
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pubmed:affiliation |
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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