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慢性関節リウマチの病態の免疫学的解析と治療への考察(免疫学の進歩-基礎と臨床-,シンポジウム,東京女子医科大学学会第308回例会)
http://hdl.handle.net/10470/23834
http://hdl.handle.net/10470/2383477c74542-41eb-438c-a77d-49c4784f4549
名前 / ファイル | ライセンス | アクション |
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KJ00006025072.pdf (601.4 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2010-08-10 | |||||
タイトル | ||||||
タイトル | 慢性関節リウマチの病態の免疫学的解析と治療への考察(免疫学の進歩-基礎と臨床-,シンポジウム,東京女子医科大学学会第308回例会) | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
別タイトル | ||||||
その他のタイトル | Analysis of the Immunopathogenesis of Rheumatoid Arthritis and its Application to Novel Experimental Therapy(Advances of immunology in basic and clinical fields,Symposium) | |||||
著者名 |
針谷, 正祥
× 針谷, 正祥× 原, まさ子× 深澤, 千賀子× 柏崎, 禎夫 |
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著者別名 | ||||||
姓名 | HARIGAI, Masayoshi | |||||
著者別名 | ||||||
姓名 | HARA, Masako | |||||
著者別名 | ||||||
姓名 | FUKASAWA, Chikako | |||||
著者別名 | ||||||
姓名 | KASHIWAZAKI, Sadao | |||||
出版者 | ||||||
出版者 | 東京女子医科大学学会 | |||||
受付日付 | ||||||
日付 | 2010-08-10 | |||||
日付タイプ | Created | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0040-9022 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00161368 | |||||
書誌情報 |
東京女子医科大学雑誌 巻 67, 号 6, p. 381-387, 発行日 1997-06-25 |
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著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | In synovia of patients with rheumatoid arthritis (RA), synoviocytes and infiltrating lymphocytes produce a variety of cytokines and contribute to the immunopathogenesis of the disease. In vitro culture of rheumatoid synovial cells revealed the following results; (1) Pro-inflammatory cytokine cascade exists in rheumatoid synovia. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β locate upstream of the cascade, while IL-6, IL-8 and monocyte chemoattractant protein-1 locate downstream of it. (2) IL-4, IL-10, IL-13 and interferon-γ (IFN-γ) modulate the production of TNF-α, IL-1β, IL-1 receptor antagonist, IL-6 and IL-8 by rheumatoid synovial cells. (3) IL-10, but not IL-4, IL-13 or IFN-γ, is produced by rheumatoid synovia and IL-10 is the major anti-inflammatory cytokine in rheumatoid synovia. (4) Peptide containing nuclear localization sequence of NF-κB p50 inhibits TNF-α-induced IL-6 and IL-8 production. These data indicates that imbalance between pro- and anti-inflammatory cytokines would contribute to the persistence of synovial inflammation of RA and that NF-κB is a novel target of therapeutic approach against RA. | |||||
著者所属 | ||||||
東京女子医科大学附属膠原病リウマチ痛風センター | ||||||
著者所属 | ||||||
東京女子医科大学附属膠原病リウマチ痛風センター | ||||||
著者所属 | ||||||
東京女子医科大学附属膠原病リウマチ痛風センター | ||||||
著者所属 | ||||||
東京女子医科大学附属膠原病リウマチ痛風センター |