过敏原特异性 IgG 对 th2 介导的气道炎症发展的贡献

Journal of allergy Pub Date : 2012-01-01 Epub Date: 2012-10-21 DOI:10.1155/2012/236075
Jesse W Williams, Melissa Y Tjota, Anne I Sperling
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摘要

在人类哮喘患者和过敏动物模型中,过敏原特异性 IgG 可导致 Th2 介导的过敏性炎症。小鼠模型阐明了 IgG 和抗原呈递细胞(APC)上的 FcγR 信号在诱导气道炎症中的重要作用。这些研究表明,适应性 B 细胞反应产生的 IgG 与先天性免疫细胞上的 FcγR 信号之间存在正反馈回路。关于哮喘或过敏性肺病患者体内 IgG 和 FcγR 的研究一直存在较大争议。一些报告发现过敏原特异性 IgG 与过敏反应的严重程度有关,而另一些研究则发现 IgG 亚类 IgG4 与过敏耐受性有关。在本文中,我们回顾了相关文献,以帮助确定先天性免疫细胞上的 IgG 和 FcγR 信号转导的性质,以及它是如何促进过敏性免疫反应的发展的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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The contribution of allergen-specific IgG to the development of th2-mediated airway inflammation.

In both human asthmatics and animal models of allergy, allergen-specific IgG can contribute to Th2-mediated allergic inflammation. Mouse models have elucidated an important role for IgG and Fc-gamma receptor (FcγR) signaling on antigen presenting cells (APC) for the induction of airway inflammation. These studies suggest a positive feedback loop between IgG produced by the adaptive B cell response and FcγR signaling on innate immune cells. Studies of IgG and FcγRs in humans with asthma or allergic lung disease have been more controversial. Some reports have identified associations between allergen-specific IgG and severity of allergic responses, while other studies have found associations of IgG subclass IgG4 with allergic tolerance. In this paper, we review the literature to help define the nature of IgG and FcγR signaling on innate immune cells and how it contributes to the development of allergic immune responses.

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