Humoral and cellular responses to gliadin in wheat-dependent, exercise-induced anaphylaxis
Humoral and cellular responses to gliadin in wheat-dependent, exercise-induced anaphylaxis
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DOI：
10.1046/j.1365-2222.2003.01568.x
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发表时间：
2003-01-01
影响因子：
6.1
通讯作者：
Alenius, H
中科院分区：
文献类型：
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作者：
Lehto, M;Palosuo, K;Alenius, H
小麦依赖性运动过敏反应（WDEIA）是一种严重的过敏反应，其中小麦摄入与体育锻炼一起诱导过敏反应。我们先前已经证明WDEIA患者具有抗麦胶蛋白的IgE抗体，并鉴定出ω-5麦胶蛋白目的检测血清中醇溶蛋白特异性IgG亚类、伊加和IgE抗体，WDEIA中嗜碱性粒细胞组胺释放和细胞介导的反应。来自WDEIA患者和无小麦过敏的对照。血清抗体粗麦醇溶蛋白提取物（CGE）和纯化的ω-5麦醇溶蛋白通过ELISA和嗜碱性粒细胞的反应性组胺释放试验。麦醇溶蛋白诱导的细胞介导的反应进行了评估，淋巴细胞增殖试验，细胞因子mRNA的表达与实时定量PCR.Results所有患者WDEIA，但没有控制，有IgE抗体CGE和ω-5麦醇溶蛋白。这两种过敏原都能从WDEIA患者的嗜碱性粒细胞中释放出高水平的组胺。CGE和omega-5麦胶蛋白的伊加抗体水平在患者中显著升高，但IgG亚类抗体的分布在两组之间没有统计学显著差异。在WDEIA患者中PBMC对CGE的应答增加，并且用CGE刺激PBMC在患者和对照中均引起IL-10 mRNA的明显诱导。与对照组相比，WDEIA患者IL-10 mRNA的表达水平明显降低（P < 0.01）。结论WDEIA的发病机制中，除抗ω-5醇溶蛋白的IgE抗体外，还可能存在特异性伊加抗体。在麦胶蛋白刺激过程中PBMC中IL-10 mRNA表达的降低可能促进麦胶蛋白特异性T细胞反应的发展。
Background Wheat-dependent, exercise-induced anaphylaxis (WDEIA) is a severe allergy where wheat ingestion together with physical exercise induces anaphylaxis. We have previously shown that patients with WDEIA have IgE antibodies against gliadin proteins and identified omega-5 gliadin (Tri a 19) as a major allergen.Objective The aim of this study was to examine gliadin-specific IgG subclass, IgA and IgE antibodies, basophil histamine release and cell-mediated responses in WDEIA.Methods Sera and peripheral blood mononuclear cells (PBMC) were obtained from patients with WDEIA and from controls without wheat allergy. Serum antibodies to crude gliadin extract (CGE) and purified omega-5 gliadin were measured by ELISA and basophil reactivity by histamine-release test. Gliadin-induced cell-mediated responses were assessed by lymphocyte proliferation assay, and cytokine mRNA expression with real-time quantitative PCR.Results All patients with WDEIA, but none of the controls, had IgE antibodies to CGE and omega-5 gliadin. Both allergens released high levels of histamine from the basophils of patients with WDEIA. Levels of IgA antibodies to CGE and omega-5 gliadin were significantly elevated in the patients, but the distribution of IgG subclass antibodies showed no statistically significant differences between the two groups. Proliferative responses of PBMC to CGE were increased in patients with WDEIA, and stimulation of PBMC with CGE caused, both in patients and in controls, a clear induction of IL-10 mRNA. Compared with the controls, induction of IL-10 mRNA expression in patients with WDEIA was significantly (P < 0.01) suppressed.Conclusion These results suggest that, in addition to IgE antibodies against omega-5 gliadin, specific IgA antibodies may be involved in the pathogenesis of WDEIA. Decreased expression of IL-10 mRNA in PBMC during gliadin stimulation may facilitate the development of gliadin-specific T cell responses.