Gour Naina, Lajoie Stephane
Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD, 21205, USA.
Curr Allergy Asthma Rep. 2016 Sep;16(9):65. doi: 10.1007/s11882-016-0640-7.
Allergic diseases, which have escalated in prevalence in recent years, arise as a result of maladaptive immune responses to ubiquitous environmental stimuli. Why only certain individuals mount inappropriate type 2 immune responses to these otherwise harmless allergens has remained an unanswered question. Mounting evidence suggests that the epithelium, by sensing its environment, is the central regulator of allergic diseases. Once considered to be a passive barrier to allergens, epithelial cells at mucosal surfaces are now considered to be the cornerstone of the allergic diathesis. Beyond their function as maintaining barrier at mucosal surfaces, mucosal epithelial cells through the secretion of mediators like IL-25, IL-33, and TSLP control the fate of downstream allergic immune responses. In this review, we will discuss the advances in recent years regarding the process of allergen recognition and secretion of soluble mediators by epithelial cells that shape the development of the allergic response.
过敏性疾病近年来患病率不断上升,是对普遍存在的环境刺激产生适应性免疫反应的结果。为什么只有某些个体对这些原本无害的过敏原产生不适当的2型免疫反应,这仍然是一个未解之谜。越来越多的证据表明,上皮细胞通过感知其环境,是过敏性疾病的核心调节因子。黏膜表面的上皮细胞曾被认为是对过敏原的被动屏障,现在则被视为过敏素质的基石。除了在黏膜表面维持屏障的功能外,黏膜上皮细胞通过分泌IL-25、IL-33和TSLP等介质,控制下游过敏性免疫反应的命运。在这篇综述中,我们将讨论近年来关于上皮细胞识别过敏原和分泌可溶性介质从而影响过敏反应发展过程的研究进展。