Asthma is an immunological disease with multiple inflammatory and clinical phenotypes, characterized by symptoms of wheezing, shortness of breath, and coughing due to airway hyperreactivity (AHR) and reversible airway obstruction. In allergic asthma, the most common form of asthma, airway inflammation is mediated by adaptive immune recognition of protein allergens by Th2 cells, resulting in airway eosinophilia. However, in other forms of asthma, inflammation is associated with immune responses to respiratory infections and airway neutrophilia. A central feature common to all forms of asthma is AHR, the heightened responsiveness of the airways to nonspecific stimuli. AHR has been shown recently in animal models of asthma to require the presence of CD1d-restricted, invariant T cell receptor-positive, natural killer T (iNKT) cells. Although allergen-specific Th2 cells and iNKT cells have many phenotypic similarities (e.g., expression of CD4 and production of Th2 cytokines), they have complementary activities, such as production of Th2 cytokines under different conditions, differential sensitivity to corticosteroids, and responsiveness to different classes of antigen (proteins versus glycolipids). We hypothesize that Th2 cells and iNKT cells interact synergistically to induce asthma but that different forms of asthma result from distinct roles of CD4(+) iNKT cells versus Th2 cells.

中文翻译：

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T细胞和NKT细胞在哮喘发病机制中的作用。

哮喘是一种免疫性疾病，具有多种炎症和临床表型，其特征是气道高反应性（AHR）和可逆性气道阻塞引起的喘息、气短和咳嗽症状。在过敏性哮喘（最常见的哮喘形式）中，气道炎症由 Th2 细胞对蛋白质过敏原的适应性免疫识别介导，导致气道嗜酸性粒细胞增多。然而，在其他形式的哮喘中，炎症与呼吸道感染和气道中性粒细胞增多的免疫反应有关。所有形式的哮喘共有的一个核心特征是 AHR，即气道对非特异性刺激的反应性增强。最近在哮喘动物模型中显示 AHR 需要存在 CD1d 限制的、不变的 T 细胞受体阳性的自然杀伤 T (iNKT) 细胞。尽管过敏原特异性 Th2 细胞和 iNKT 细胞有许多表型相似之处（例如，CD4 的表达和 Th2 细胞因子的产生），但它们具有互补的活性，例如在不同条件下产生 Th2 细胞因子、对皮质类固醇的不同敏感性以及对不同细胞因子的反应性。抗原类别（蛋白质与糖脂）。我们假设 Th2 细胞和 iNKT 细胞协同相互作用以诱发哮喘，但不同形式的哮喘是由 CD4(+) iNKT 细胞与 Th2 细胞的不同作用引起的。和对不同类别抗原的反应（蛋白质与糖脂）。我们假设 Th2 细胞和 iNKT 细胞协同相互作用以诱发哮喘，但不同形式的哮喘起因于 CD4(+) iNKT 细胞与 Th2 细胞的不同作用。和对不同类别抗原的反应性（蛋白质与糖脂）。我们假设 Th2 细胞和 iNKT 细胞协同相互作用以诱发哮喘，但不同形式的哮喘起因于 CD4(+) iNKT 细胞与 Th2 细胞的不同作用。