Division of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Mucosal Immunol. 2010 Mar;3(2):104-10. doi: 10.1038/mi.2009.138. Epub 2009 Dec 23.
Allergic diseases, which have reached epidemic proportions, are caused by inappropriate immune responses to a relatively small number of environmental proteins. The molecular basis for the propensity of specific proteins to promote maladaptive, allergic responses has been difficult to define. Recent data suggest that the ability of such proteins to promote allergic responses in susceptible hosts is a function of their ability to interact with diverse pathways of innate immune recognition and activation at mucosal surfaces. This review highlights recent insights into innate immune activation by allergens--through proteolytic activity, engagement of pattern recognition receptors, molecular mimicry of TLR signaling complex molecules, lipid-binding activity, and oxidant potential--and the role of such activation in inducing allergic disease. A greater understanding of the fundamental origins of allergenicity should help define new preventive and therapeutic targets in allergic disease.
过敏疾病已达到流行程度，是由对相对少数环境蛋白的不适当免疫反应引起的。特定蛋白质促进适应性过敏反应的倾向的分子基础一直难以确定。最近的数据表明，这些蛋白质在易感宿主中促进过敏反应的能力是其与粘膜表面固有免疫识别和激活的多种途径相互作用的功能。这篇综述强调了过敏原通过蛋白水解活性、模式识别受体的结合、TLR 信号复合物分子的分子模拟、脂质结合活性和氧化潜力引起固有免疫激活的最新见解，以及这种激活在诱导过敏疾病中的作用。对变应原性的基本起源有更深入的了解，应有助于确定过敏疾病的新的预防和治疗靶点。
