Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390-9063, USA.
Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Curr Allergy Asthma Rep. 2017 Feb;17(2):9. doi: 10.1007/s11882-017-0677-2.
Multiple clinical and epidemiological studies demonstrate links between allergic sensitization and virus-induced atopic disease exacerbations. This review summarizes the recent findings regarding allergen, viral, and host cellular mechanisms relevant to these observations.
Recent studies have focused on the molecular pathways and genetic influences involved in allergen-mediated inhibition of innate antiviral immune responses. Multiple tissue and cell types from atopic individuals across the atopy spectrum exhibit deficient interferon responses to a variety of virus infections. Impairment in barrier function, viral RNA and DNA recognition by intracellular sensing molecules, and dysregulation of signaling components are broadly affected by allergic sensitization. Finally, genetic predisposition by numerous nucleotide polymorphisms also impacts immune pathways and potentially contributes to virus-associated atopic disease pathogenesis. Allergen-virus interactions in the setting of atopy involve complex tissue and cellular mechanisms. Future studies defining the pathways underlying these interactions could uncover potential therapeutic targets. Available data suggest that therapies tailored to restore specific components of antiviral responses will likely lead to improved clinical outcomes in allergic disease.
多项临床和流行病学研究表明过敏致敏与病毒诱导的特应性疾病加重之间存在关联。本综述总结了与这些观察结果相关的过敏原、病毒和宿主细胞机制的最新发现。
最近的研究集中在涉及过敏原介导的先天抗病毒免疫反应抑制的分子途径和遗传影响上。特应性谱中来自特应性个体的多种组织和细胞类型对多种病毒感染表现出干扰素反应不足。过敏致敏广泛影响屏障功能、细胞内感应分子对病毒 RNA 和 DNA 的识别以及信号成分的失调。最后,许多核苷酸多态性的遗传易感性也影响免疫途径,并可能有助于病毒相关特应性疾病的发病机制。特应性背景下的过敏原-病毒相互作用涉及复杂的组织和细胞机制。未来研究确定这些相互作用的途径可能会揭示潜在的治疗靶点。现有数据表明,针对恢复抗病毒反应特定成分的治疗方法可能会改善过敏疾病的临床结局。