Serum IgE response to orally ingested antigen: a novel IgE response model with allergen-specific T-cell receptor transgenic mice.

Serum IgE response to orally ingested antigen: a novel IgE response model with allergen-specific T-cell receptor transgenic mice.
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对口服摄入抗原的血清 IgE 反应:一种采用过敏原特异性 T 细胞受体转基因小鼠的新型 IgE 反应模型。

DOI:
10.1067/mai.2000.104934
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发表时间:
2000
期刊:
The Journal of allergy and clinical immunology
影响因子:
--
通讯作者:
S. Kaminogawa
S. Kaminogawa
中科院分区:
--
文献类型:
--
作者:
K. Shida;S. Hachimura;A. Ametani;M. Ishimori;M. Ling;M. Hashiguchi;Y. Ueda;T. Sato;Y. Kumagai;K. Takamizawa;S. Habu;S. Kaminogawa

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背景 口服过敏原引起IgE反应的机制尚不清楚,因为很少有动物模型可用于研究这种反应。 目的 我们试图开发一种小鼠模型,适合于研究IgE对口服摄入过敏原的反应,这将使我们能够识别能够促进IgE产生的T细胞。 方法 卵清蛋白(OVA)特异性T细胞受体转基因小鼠喂养的饮食含有OVA,血清抗体反应和脾细胞产生的细胞因子进行了检查。 结果 转基因小鼠口服OVA导致血清中抗原特异性IgE和总IgE水平升高。随后用OVA静脉内攻击OVA喂养的转基因小鼠导致过敏性休克。通过脾细胞的细胞因子产生的分析揭示,在开始饲喂OVA饮食后1周,在脾中出现高IL-4产生性T细胞。发现来自这些小鼠的T细胞在体外促进BALB/c B细胞的IgE分泌。这种辅助活性和IL-4分泌水平在长期喂养后减少。这些发现表明口服摄入的抗原引起产生高水平T(H2)型细胞因子并促进IgE分泌的T细胞亚群的应答的可能性,并且这些相同的T细胞被口服摄入的抗原耐受。 结论 这种转基因小鼠的实验模型可能是一个有用的工具,为进一步研究的细胞和分子机制的T细胞和IgE应答口服摄入的抗原。
BACKGROUND The mechanism by which orally ingested allergens elicit an IgE response remains unclear because there are few animal models available for investigation of this response. OBJECTIVE We tried to develop a murine model suitable for investigation of the IgE response to orally ingested allergens, which would allow us to identify T cells that could promote IgE production. METHODS Ovalbumin (OVA)-specific T-cell receptor transgenic mice were fed a diet containing OVA, and both the serum antibody response and cytokine production by splenocytes were examined. RESULTS Oral administration of OVA to transgenic mice led to an increase in the levels of both antigen-specific IgE and total IgE in the sera. Subsequent intravenous challenge of OVA-fed transgenic mice with OVA resulted in anaphylactic shock. Analysis of cytokine production by splenocytes revealed that high IL-4-producing T cells appeared in the spleen 1 week after the start of feeding the OVA diet. T cells from these mice were found to promote IgE secretion by BALB/c B cells in vitro. This helper activity and the levels of IL-4 secretion were diminished after long-term feeding. These findings suggest the possibility that the orally ingested antigen elicited a response by a subpopulation of T cells that produce high levels of T(H2)-type cytokines and that promote IgE secretion, and these same T cells were tolerized by the orally ingested antigen. CONCLUSION This experimental model with transgenic mice may be a useful tool for further studies of the cellular and molecular mechanisms of the T-cell and IgE responses to orally ingested antigens.
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