哮喘致病过程中天然免疫和过继性免疫的相互作用：有关哮喘急性发作的研究新观点
2010/08/11
哮喘是一种复杂的多基因疾病。最常见的类型是过敏性哮喘，常见于儿童和青年，这也是本综述的重点。过敏性哮喘的主要危险因素是对持续吸入过敏原的致敏，而不能产生保护性免疫耐受。该耐受过程受到气道粘膜树突状细胞的调节，正常情况下，该耐受过程能导致调节性T细胞的程序化变化，而后抑制Th2记忆细胞的活化，驱动IgE的产生，针对IgE介导的组织损伤产生效应细胞群。越来越多的证据都强调了该过程的复杂性，特别是天然免疫和过继性免疫的相互作用导致该过程的反复，两者的相互作用使得每个来源于细胞腔室的信号都会产生相应的免疫应答。此外，局部的间质细胞也能整合信号，很好的调节免疫反应，满足局部微环境的需求，这使得该过程更为复杂。天然免疫与过继性免疫之间平衡的紊乱，被越来越多的研究认为是很多疾病发生的基础，特别是过敏性哮喘。由病毒感染导致的哮喘加重就是一个很好的例子。
（林江涛 审校）
J Allergy Clin Immunol. 2010 May;125(5):963-72; quiz 973-4. Epub 2010 Apr 15.
Interactions between innate and adaptive immunity in asthma pathogenesis: new perspectives from studies on acute exacerbations.
Holt PG, Strickland DH.
Telethon Institute for Child Health Research and the Centre for Child Health Research, Faculty of Medicine and Dentistry, University of Western Australia, Perth, Australia. patrick@ichr.uwa.edu.au
Abstract
Asthma is a complex multigenic disease. The most frequently encountered form is atopic asthma, which is at its highest prevalence during childhood/young adulthood, and this represents the main focus of this review. The primary risk factor for atopic asthma is sensitization to perennial aeroallergens resulting from a failure to generate protective immunologic tolerance. This tolerance process is orchestrated by airway mucosal dendritic cells and normally results in programming of regulatory T cells, which inhibit activation of the T(H)2 memory cells that, among other activities, drive IgE production and prime the effector populations responsible for IgE-mediated tissue damage. Emerging evidence highlights the complexity of this process, in particular the iterative nature of the underlying interactions between innate and adaptive immune mechanisms in which virtually every signal emanating from one cellular compartment provokes an answering response from the other. To further complicate this picture, the local mesenchyme can also interpose signals to fine tune immune responses to optimally meet local microenvironmental needs. Perturbation of the balance between these interlinked innate and adaptive immune pathways is increasingly believed to be the basis for disease expression, and in the specific case of atopic asthma, the prototypic example of this (discussed below) is acute exacerbations triggered by viral infections.
J Allergy Clin Immunol. 2010 May;125(5):963-72; quiz 973-4. Epub 2010 Apr 15.
（林江涛 审校）
J Allergy Clin Immunol. 2010 May;125(5):963-72; quiz 973-4. Epub 2010 Apr 15.
Interactions between innate and adaptive immunity in asthma pathogenesis: new perspectives from studies on acute exacerbations.
Holt PG, Strickland DH.
Telethon Institute for Child Health Research and the Centre for Child Health Research, Faculty of Medicine and Dentistry, University of Western Australia, Perth, Australia. patrick@ichr.uwa.edu.au
Abstract
Asthma is a complex multigenic disease. The most frequently encountered form is atopic asthma, which is at its highest prevalence during childhood/young adulthood, and this represents the main focus of this review. The primary risk factor for atopic asthma is sensitization to perennial aeroallergens resulting from a failure to generate protective immunologic tolerance. This tolerance process is orchestrated by airway mucosal dendritic cells and normally results in programming of regulatory T cells, which inhibit activation of the T(H)2 memory cells that, among other activities, drive IgE production and prime the effector populations responsible for IgE-mediated tissue damage. Emerging evidence highlights the complexity of this process, in particular the iterative nature of the underlying interactions between innate and adaptive immune mechanisms in which virtually every signal emanating from one cellular compartment provokes an answering response from the other. To further complicate this picture, the local mesenchyme can also interpose signals to fine tune immune responses to optimally meet local microenvironmental needs. Perturbation of the balance between these interlinked innate and adaptive immune pathways is increasingly believed to be the basis for disease expression, and in the specific case of atopic asthma, the prototypic example of this (discussed below) is acute exacerbations triggered by viral infections.
J Allergy Clin Immunol. 2010 May;125(5):963-72; quiz 973-4. Epub 2010 Apr 15.
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糖皮质激素保护长效β2-肾上腺素受体激动剂促哮喘作用的机制研究
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病毒在急性哮喘加重中的作用
