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内在的危险:内源性危险信号、特应性和哮喘。

The danger within: endogenous danger signals, atopy and asthma.

作者信息

Willart M A M, Lambrecht B N

机构信息

Laboratory of Immunoregulation and Mucosal Immunity, Department of Pulmonary Medicine, Ghent University, Ghent, Belgium.

出版信息

Clin Exp Allergy. 2009 Jan;39(1):12-9. doi: 10.1111/j.1365-2222.2008.03118.x. Epub 2008 Oct 30.

Abstract

In allergic asthmatics, airway inflammation is triggered by specific (inhalation of allergen such as house dust mite allergen and pollen spores) or non-specific triggers (such as air pollutants and viral infection). Most of these inhaled particles are immunologically inert. Dendritic cells (DCs) are essential for priming and T helper-2 differentiation of naïve T cells towards aeroallergens. Contamination of antigens with pattern-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), is required to activate DCs to mount an immune response. Damage-associated molecular patterns (DAMPs), such as uric acid and adenosine triphosphate (ATP), also contribute to the induction of inflammation by activation and recruitment of various inflammatory cells. Compelling evidence suggests that a tight collaboration between PAMPs and DAMPs is needed to start an immune response to allergens. Several studies have recently demonstrated an important role of endogenous danger signals at the inception and maintenance phase of allergic disease. Further research into this area should focus on the possible role of these factors in maintenance of chronic disease and induction of airway remodelling.

摘要

在过敏性哮喘患者中,气道炎症由特异性触发因素(如吸入屋尘螨过敏原和花粉孢子等过敏原)或非特异性触发因素(如空气污染物和病毒感染)引发。这些吸入颗粒大多在免疫方面呈惰性。树突状细胞(DCs)对于初始T细胞针对气源性过敏原的启动和向辅助性T细胞2分化至关重要。抗原需与模式相关分子模式(PAMPs)如脂多糖(LPS)发生污染,才能激活DCs以引发免疫反应。损伤相关分子模式(DAMPs)如尿酸和三磷酸腺苷(ATP),也通过激活和募集各种炎症细胞促进炎症的诱导。有力证据表明,PAMPs和DAMPs之间需要紧密协作才能启动针对过敏原的免疫反应。最近的几项研究表明内源性危险信号在过敏性疾病的起始和维持阶段发挥重要作用。该领域的进一步研究应聚焦于这些因素在维持慢性疾病和诱导气道重塑方面的可能作用。

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