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在感染皮螨的小鼠中诱导IgE及过敏样反应。

Induction of IgE and allergic-type responses in fur mite-infested mice.

作者信息

Pochanke Veronika, Hatak Sarah, Hengartner Hans, Zinkernagel Rolf M, McCoy Kathy D

机构信息

Institute of Experimental Immunology, University Hospital Zurich, Zurich, Switzerland.

出版信息

Eur J Immunol. 2006 Sep;36(9):2434-45. doi: 10.1002/eji.200635949.

DOI:10.1002/eji.200635949
PMID:16909433
Abstract

High serum IgE levels are characteristic of allergic diseases and immune responses to nematode parasites. A murine allergy model based on infestation with the fur mites Myocoptes musculinus and Myobia musculi was investigated. Analysis of mite infestation in various knockout mice revealed that IgE production in response to these ectoparasites was dependent on T cells, IL-4, and CD40L. Secretion of IL-4 by CD4+ T cells obtained from peripheral LN draining mite-infested skin sites was increased with progressing mite infestation and correlated with the serum IgE induction. A time course analysis of the mRNA expression of switched IgE, activation-induced cytidine deaminase (AID), and epsilon germ-line transcripts (epsilonGLT) suggested that switching to IgE in response to fur mites occurred initially in skin-draining LN. In addition, mite infestation induced mast cell degranulation in the skin as well as mast cell infiltration into skin-draining LN. Analysis of the immune response generated in mite-infested mice is a valuable model for the investigation of allergic disorders and provides information for better understanding of mechanisms involved in IgE induction and regulation in a physiological way of allergen-exposure resembling atopic sensitization in humans.

摘要

高血清IgE水平是过敏性疾病和对线虫寄生虫免疫反应的特征。研究了一种基于感染皮螨肌螨(Myocoptes musculinus)和肌鼠螨(Myobia musculi)的小鼠过敏模型。对各种基因敲除小鼠的螨感染分析表明,对这些体外寄生虫的IgE产生依赖于T细胞、IL-4和CD40L。从螨感染皮肤部位引流的外周淋巴结获得的CD4 + T细胞分泌的IL-4随着螨感染的进展而增加,并与血清IgE诱导相关。对转换型IgE、活化诱导的胞苷脱氨酶(AID)和ε种系转录本(εGLT)mRNA表达的时间进程分析表明,对皮螨的IgE转换最初发生在皮肤引流淋巴结。此外,螨感染诱导皮肤中的肥大细胞脱颗粒以及肥大细胞浸润到皮肤引流淋巴结。对螨感染小鼠产生的免疫反应进行分析是研究过敏性疾病的有价值模型,并为以类似于人类特应性致敏的过敏原暴露生理方式更好地理解IgE诱导和调节机制提供信息。

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