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Co-operative analysis for pathogenesis and prediction of kawasaki disease

Research Project

Project/Area Number 05670714
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Pediatrics
Research InstitutionKurume University

Principal Investigator

SAKAGUCHI Hinako (1994)  Kurume University Medicine Research Associate, 医学部, 助手 (50258422)

井上 治 (1993)  久留米大学, 医学部, 講師 (20193576)

Co-Investigator(Kenkyū-buntansha) NISHIYORI Astushi  Kurume University Medicine Research Associate, 医学部, 助手 (30218226)
KATO Hirohisa  Kurume University Medicine Professor, 医学部, 教授 (30080724)
坂口 美奈子  久留米大学, 医学部, 助手 (50258422)
佐藤 登  久留米大学, 医学部, 助手 (50205952)
Project Period (FY) 1993 – 1994
Project Status Completed (Fiscal Year 1994)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
Keywordskawasaki disease / Superantigen / TNF-alpha / 接着分子 / サイトカイン
Research Abstract

It has been recently reported that KD is associated with the selective expansion of vbeta2^+ and vbeta8.1^+ T cells in peripheral blood lymphocytes (PBL) by studying the T cell receptor (TCR) repertoire of in vitro activated T cells, and therefore, KD may be caused by a superantigen. To better understand immunopathology of KD,we have inestigated TCR Vbeta2 and Vbeta8.1 expression on both the T cells of freshly isolated PBL and T cell clones (TCC) from patients with KD.Cytokine production by TCC was also studied. Blood samples were obtained from patients with acute (n=20) and convalescent (n=20) KD,age-matched children with non-infectious diseases (n=18) and healthy adults (n=20). Among these four groups, there were no significant differences in the percentages of either Vbeta2^+ or Vbeta8.1^+ T cells of freshly isolated PBL.The same was true for the CD4^+ or CD8^+ T cell subsets. One hundred-five TCC (98 CD3^+ CD4^+ CD8^- and 7 CD3^+ CD4^- CD8^+) established from the affected skin, lymph node or PBL of six patients with KD were also negative for either Vbeta2 or Vbeta8.1 TCR.Sixty-eight of 105 TCC (65%) produced detectable levels (>5 pg per ml) of tumor necrosis factor-alpha (TNF-alpha) (6-1016 pg per ml), in the absence of any stimuli. In contrast, only 11 (10%) of 105 TCC or 7 (7%) of 97 TCC produced detectable levels of IL-2 or IL-6, respectively, in the absence of any stimuli. Stimulation with PHA and PMA induced the majority of TCC to produce higher amounts of TNF-alpha、IL-2 and IL-6.These results suggest that CD4^+ T helper cells expressing TCR-beta other than Vbeta2 or Vbeta8 receptor, primarily through TNF-alpha production, are involved in the immunopathology of KD.

Report

(3 results)
  • 1994 Annual Research Report   Final Research Report Summary
  • 1993 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] M.SAKAGUCHI: "characterization of DC4^+T helpes cells in patients with kawasaki disease" Clinical Experimental Immunology. 99. 276-282 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] M.SAKAGUCHI et al.: "characterization of CD4^+ T helper cells in patients with kawasaki disease" clinical Experimental Immunology. 99. 276-282 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] M.SAKAGUCHI: "characterization of CD4^+Thelper cells in patients with kawasaki disea" climical Experimental Immunology. 99. 276-282 (1995)

    • Related Report
      1994 Annual Research Report
  • [Publications] Atsushi Nishiyori: "Toxic shock syndrome toxin-secreting Staphylococcus aureus in Kawasaki syndrome" Lancet. 343. 299-300 (1994)

    • Related Report
      1993 Annual Research Report

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Published: 1993-04-01   Modified: 2016-04-21  

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