| Project/Area Number |
04454250
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | University of Tokyo |
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Principal Investigator |
ITO Koji University of Tokyo, Faculty of Medicine, professor, 医学部(病), 教授 (10008310)
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| Co-Investigator(Kenkyū-buntansha) |
MORITA Yutaka Univ. of Tokyo, Faculty of Medicine, associate prof., 医学部(病), 助教授 (60107620)
TAKIZAWA Hajime Univ. of Tokyo, Faculty of Medicine, assistant prof., 医学部(病), 助手 (80171578)
MORI Akio Univ. of Tokyo, Faculty of Medicine, assistant professor, 医学部(病), 助手 (80251247)
SUKO Mastunobu Univ. of Tokyo, Faculty of Medicine, lecturer, 医学部(病), 講師 (80107622)
OKUDAIRA Hirokazu Univ. of Tokyo, Faculty of Medicine, lecturer, 医学部(病), 講師 (30106645)
高石 敏昭 東京大学, 医学部(病), 助手 (40154736)
平井 浩一 東京大学, 医学部(病), 助手 (10156630)
灰田 美知子 東京大学, 医学部(病)物療内科, 医員 (90240712)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1993: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1992: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | Bronchial asthma / T cell / eosinophil / Interleukin-5 / T cell clone / アレルギー / インターロイキン5 / T cell clone / アレルゲン / Der f II / T cell / ハウスダストマイト |
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| Research Abstract |
Chronic eosinophilic inflammation of bronchial mucosa has been recognized in the pathophysilology of bronchial asthma. The roles of T cells and T cell cytokines, including especially IL-5, have been strongly implicated in the local infiltration and activation of eosinophils. We have indicated that enhanced IL-5 production by CD4^+ T cells is observed in both atopic and non-atopic (intrinsic) asthmatics. Control of IL-5 production by activated T cells must be a beneficial approach to manage allergic diseases characterized by eosinophilic inflammation. In order to delineate the precise mechanisms of IL-5 production by human "allergic" T cells, we established T cell clones from asthmatic patitents and analyzed cytokine production by those helper T cell clones. Both PKC activation and Ca^<++> influx were required for IL-5 synthesis. The transcription factors, NF-AT and AP-1 were suggested to be involved in IL-5 gene transcription. IL-5 synthesis by human T cells was dependent on endogeneously produced IL-2. Human recombinant IL-2 initiated IL-5 gene transcription in IL-5 producing T cell clones. PBMC of some intrinsic asthmatics produced IL-5 in response to mite allergen extract. T cell clones established from such patients did produce IL-5 in response to mite allergen, suggesting that mite allergen might be in part responsible for so called "intrinsic" asthma.
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