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Analysis of deterioration of suppression mechanisms of auto-immunity in atopic dermatitis

Research Project

Project/Area Number 17591172
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Dermatology
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

TANAKA Toshihiko  Hiroshima University, Hospital, Lecturer, 病院, 講師 (80263705)

Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,600,000 (Direct Cost: ¥1,600,000)
Keywordsatopic dermatitis / IgE / sweat / Type I hypersensitivity / Th2 cytokines / IL-4 / IFN-γ
Research Abstract

In many of patients with atopic dermatitis, sweat is one of the most important aggravating factors. About 80% of the patients show a positive skin reaction to autologous sweat, and peripheral blood basophils release various amounts of histamine in response to sweat. These results show that the patients with atopic dermatitis show type I hypersensitivity to sweat. In recent years, we have shown that sweat-induced histamine release from basophils is mediated by IgE-antibody specific to the sweat antigen. In this study, we tried to show how mononuclear cells, including lymphocytes, will react to sweat antigen. Firstly, peripheral blood mononuclear cells (PBMCs) are incubated with the sweat antigen, and proliferation and cytokine production of these cells were examined. Proliferation of PBMCs was enhanced more by the sweat antigen in patients with atopic dermatitis than in healthy volunteers, but the difference was not statistically significant. IL-4 production by PBMCs in response to the sweat antigen and house dust mite allergen (Derf1) was more in atopic dermatitis patients than in healthy volunteers with statistical significance. On the other hand, interferon-gamma production in response to the sweat antigen was less in atopic dermatitis patients than in healthy volunteers. The same pattern reaction was seen using CD4+CD25- cells. These results show that atopic dermatitis patients show Th2-type cytokine production in response to the sweat antigen.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (4 results)

All 2007 2006

All Journal Article (4 results)

  • [Journal Article] 汗の減感作療法が奏効したコリン性蕁麻疹の1例2007

    • Author(s)
      田中稔彦, 石井香, 鈴木秀規, 亀好良一, 秀道広
    • Journal Title

      アレルギー 56(1)

      Pages: 54-57

    • NAID

      110006164372

    • Related Report
      2006 Annual Research Report
  • [Journal Article] アトピー性皮膚炎に対するシャワー浴の効果に関する調査2006

    • Author(s)
      秀道広, 亀好良一, 田中稔彦
    • Journal Title

      広島医学 59(12)

      Pages: 987-991

    • Related Report
      2006 Annual Research Report
  • [Journal Article] 汗のI型アレルギー2006

    • Author(s)
      田中稔彦
    • Journal Title

      MEDICO 37(10)

      Pages: 369-372

    • Related Report
      2006 Annual Research Report
  • [Journal Article] アトピー性皮膚炎治療薬のEBM : 抗ヒスタミン薬・抗アレルギー薬2006

    • Author(s)
      田中稔彦, 秀道広
    • Journal Title

      アレルギーの臨床 26(9)

      Pages: 688-692

    • Related Report
      2006 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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