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.

在许多特应性皮炎的患者中，汗水是最重要的加重因素之一。大约80％的患者对自体汗液表现出正面的皮肤反应，并且外周血嗜碱性粒细胞释放出各种量的组胺，以响应汗液。这些结果表明，特应性皮炎的患者表现出I型汗水的超敏反应。近年来，我们已经表明，汗液诱导的嗜嗜嗜性嗜碱性盐释放是由特异于汗液抗原的IgE抗体介导的。在这项研究中，我们试图展示包括淋巴细胞在内的单核细胞如何对汗液抗原做出反应。首先，外周血单核细胞（PBMC）与汗液抗原孵育，并检查了这些细胞的增殖和细胞因子的产生。与健康的志愿者相比，特应性皮炎患者的汗液抗原的增殖更多，但差异在统计学上并不显着。 PBMC响应于汗水和家用尘螨过敏原（DERF1）的IL-4产生的特应性皮炎患者比具有统计学意义的健康志愿者中的IL-4产生。另一方面，与健康志愿者相比，针对汗液抗原的干扰素γ响应于汗水抗原的患者的生产要少于健康志愿者。使用CD4+CD25-细胞可以看到相同的模式反应。这些结果表明，特应性皮炎患者显示出对汗液抗原的响应Th2型细胞因子的产生。