Editorial, Tumor necrosis factor alpha-mediated asthma?
Editorial, Tumor necrosis factor alpha-mediated asthma?
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社论，肿瘤坏死因子α介导的哮喘？
DOI：
10.1159/000342420
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Takeshi Nabe
中科院分区：
文献类型：
--
作者：
Yang Cao;Masanori Fujii;Keiichi Ishihara;Satoshi Akiba;Hiroyuki Yasui;Takeshi Nabe;Takeshi Nabe
根据现有的知识，过敏性哮喘的机制如下：当吸入的过敏原渗透到气道上皮时，被树突状细胞检测到，树突状细胞迁移到淋巴结，将加工后的抗原呈递给T细胞，B细胞开始产生抗原特异性免疫球蛋白E （IgE）。IgE与多种细胞类型上的fcee受体结合，包括肥大细胞和嗜碱性细胞。当过敏个体随后暴露于特定过敏原时，过敏原与细胞上的特定IgE结合，导致肥大细胞和嗜碱性细胞活化，释放化学介质，如组胺、花生四烯酸代谢物和蛋白酶进入气道组织。这些介质引起早期哮喘反应，这是过敏原暴露后30分钟内引起的气道阻塞。也有特定人群的哮喘受试者表现出较晚的哮喘反应，即在过敏原攻击后数小时引发气道阻塞并持续较长时间。晚期哮喘反应被认为是基于Th2细胞和嗜酸性粒细胞[1]介导的气道炎症。除了早期和晚期的哮喘反应外，th2偏倚的气道炎症会导致气道对非特异性刺激的高反应性（AHR）和气道组织的结构重塑。各种实验模型再现了哮喘的这些表型。
According to established knowledge, the mechanisms of allergic asthma are as follows: when an inhaled allergen penetrates the airway epithelium, it is detected by dendritic cells, which migrate to the lymph node and present the processed antigen to T cells, and B cells start to produce antigen-specific immunoglobulin E (IgE). IgE binds to Fcε receptors on a variety of cell types including mast cells and basophils. When an allergic individual is subsequently exposed to the specific allergen, the allergen binds to the specific IgE on the cells, causing activation of mast cells and basophils to release chemical mediators, such as histamine, arachidonic acid metabolites and proteases into the airway tissue. These mediators cause an early asthmatic response, which is an airway obstruction induced within 30 min after allergen exposure. There is also a specific population of asthmatic subjects which exhibits a late asthmatic response, ie an airway obstruction triggered several hours after allergen challenge and persisting for a relatively long time.The late asthmatic response has been thought to be based on airway inflammation orchestrated by Th2 cells and eosinophils [1]. In addition to the early and late asthmatic responses, Th2-biased airway inflammation leads to airway hyperresponsiveness (AHR) to nonspecific stimuli and structural remodeling of airway tissues. Various experimental models reproduce these phenotypes of asthma.