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The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation

机译:过敏原特异性IgG对Th2介导的气道炎症发展的贡献

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摘要

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.
机译:在人类哮喘和动物过敏模型中,过敏原特异性IgG均可导致Th2介导的过敏性炎症。小鼠模型阐明了抗原呈递细胞(APC)上的IgG和Fc-γ受体(FcγR)信号转导对于诱导气道炎症的重要作用。这些研究表明,由适应性B细胞反应产生的IgG与先天免疫细胞上的FcγR信号传导之间存在正反馈回路。在患有哮喘或过敏性肺病的人中对IgG和FcγR的研究更具争议性。一些报告确定了过敏原特异性IgG与过敏反应严重程度之间的关联,而其他研究则发现IgG4亚类IgG与过敏耐受性相关。在本文中,我们回顾了文献,以帮助定义先天免疫细胞上IgG和FcγR信号传导的性质以及其如何促进过敏性免疫反应的发展。

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