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Molecular and pathological analysis of CVD-interstitial pneumonia by using lung tissue-infiltrating T lymphocytes

Research Project

Project/Area Number 14570561
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionDokkyo University School of Medicine

Principal Investigator

TAKEDA Akira  Dokkyo University School of Medicine, Dept. of Medicine, Assistant professor, 医学部, 講師 (90155002)

Co-Investigator(Kenkyū-buntansha) 福島 康次  獨協医科大学, 医学部, 講師 (00254996)
沼尾 利郎  獨協医科大学, 医学部, 講師 (60172748)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000)
KeywordsInterstitial pneumonia / Collagen diseases / T cells
Research Abstract

Interstitial pneumonia (IP) associated with polymyositis/dermatomyositis (PM/DM) has been perceived as an life-threatening complication of the connective tissue disease.
Since the pathogenesis of IP remains unclear, the treatment has been conventional and often inadequate.
However, the precise characterization of the lymphocytes infiltrating the lung tissue may provide clue to understanding the immune-mediated mechanisms for IP.
We examined the phenotypic profiles of lung tissue-infiltrating lymphocytes as well as the expression of cytokines in the affected lung tissue.
TCR-repertoire study with RT-PCR was also employed using lung derived RNA and the results suggested oligoclonal expansion of particular T cell populations.
Immunohistochemical analysis of VATS biopsies from eight patients with PM/DM demonstrated that the lymphocytes in the lesions are predominantly T cells a most of which are CD4 positive, and the study also showed strong expression of IFNγ in the tissue with lesser levels of 1L4 and 1L5.
These data suggest that the pivotal role of T cells which may contribute to the development of IP associated with PM/DM through the proinflammatory cytokine-mediated mechanism.

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] Arakawa H, et al.: "HSIP associated with PM/Dm."Chest. 123. 1096-1103 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 武田 昭, 他: "T細胞レセプター可変領域の解析・膠原病性間質性肺炎"分子呼吸器病. 7. 147-153 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 武田 昭, 他: "肺浸潤T細胞による膠原病性間質性肺炎の病態解析"RMCB研究会. 23. 43-47 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Arakawa H, Yamada H, Kurihara Y, Nakajima Y, Takeda A, Fukushima Y, Fujioka M: "Nonspecific interstitial pneumonia associated with plymyositis and dermatomyositis"Chest. 123. 1096-1103 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Arakawa, H., et al.: "NSIP associated with PM and DM."Chest. 123. 1096-1103 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 武田 昭: "T細胞レセプター可変領域の解析・膠原病性間質性肺炎"分子呼吸器病. 7. 147-153 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] 武田 昭: "T細胞レセプター可変領域の解析によりantigen-driven mechanismによる肺病変発現機序が示唆された膠原病性間質性肺炎"分子呼吸器病. 7巻・2号. 69-75 (2003)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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