Division of Molecular Immunology, Department of Pediatrics, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, Ohio.
J Allergy Clin Immunol. 2010 May;125(5):955-60; quiz 961-2. doi: 10.1016/j.jaci.2010.03.002. Epub 2010 Apr 9.
Why specific, ubiquitous, otherwise innocuous environmental proteins tend to provoke maladaptive, T(H)2-polarized immune responses in susceptible hosts is a fundamental mechanistic question for those interested in the pathogenesis, therapy, and prevention of allergic disease. The current renaissance in the study of innate immunity has provided important insights into this question. The theme emerging from recent studies is that direct (dys)functional interactions with pathways of innate immune activation that evolved to signal the presence of microbial infection are central to the molecular basis for allergenicity. This article reviews these data.
为什么特定的、普遍存在的、原本无害的环境蛋白往往会在易感性宿主中引发适应性不良、T(H)2 极化的免疫反应，这是对过敏疾病的发病机制、治疗和预防感兴趣的人需要解决的一个基本机制问题。目前对先天免疫的研究复兴为这个问题提供了重要的见解。最近的研究中出现的主题是，与先天免疫激活途径的直接（功能障碍）相互作用，这些途径的进化是为了信号微生物感染的存在，这是变应原性的分子基础的核心。本文综述了这些数据。
