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

特应性皮炎自身免疫抑制机制恶化分析

基本信息

批准号：
17591172
负责人：
TANAKA Toshihiko
金额：
$ 1.79万
依托单位：
HIROSHIMA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17591172/
关键词：
atopic dermatitis IgE sweat Type I hypersensitivity Th2 cytokines IL-4 IFN-γ

项目摘要

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.

在许多特应性皮炎患者中，汗液是最重要的加重因素之一。大约80%的患者对自体汗液显示出阳性皮肤反应，外周血嗜碱性粒细胞对汗液有反应，释放不同数量的组胺。这些结果表明，特应性皮炎患者对汗液表现出I型超敏反应。近年来，我们发现汗液诱导的嗜碱性粒细胞组胺释放是由汗液抗原特异性IgE抗体介导的。在这项研究中，我们试图展示单核细胞，包括淋巴细胞，将如何对汗液抗原作出反应。首先，将外周血单个核细胞（PBMC）与汗液抗原一起孵育，并检查这些细胞的增殖和细胞因子产生。特应性皮炎患者外周血单个核细胞的增殖能力较健康志愿者明显增强，但差异无统计学意义。特应性皮炎患者PBMC对汗液抗原和屋尘螨变应原（Derf 1）的IL-4产生量高于健康志愿者，具有统计学意义。另一方面，特应性皮炎患者对汗液抗原产生的干扰素-γ比健康志愿者少。使用CD 4 + CD 25-细胞观察到相同的模式反应。这些结果表明，特应性皮炎患者显示Th 2型细胞因子产生应答汗液抗原。