2006 Fiscal Year Final Research Report Summary
Analysis of deterioration of suppression mechanisms of auto-immunity in atopic dermatitis
| Project/Area Number |
17591172
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
TANAKA Toshihiko Hiroshima University, Hospital, Lecturer, 病院, 講師 (80263705)
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| Project Period (FY) |
2005 – 2006
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| Keywords | atopic dermatitis / IgE / sweat / Type I hypersensitivity / Th2 cytokines / IL-4 / IFN-γ |
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| 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.
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