Meakins-Christie Laboratories, Department of Medicine, McGill University, 3626 St. Urbain, Montreal, Quebec H2X 2P2, Canada.
Curr Opin Pharmacol. 2010 Jun;10(3):218-25. doi: 10.1016/j.coph.2010.03.004. Epub 2010 Apr 19.
Asthma is an inflammatory disease which is associated with activated T cells in the airway wall. The contribution of the T lymphocyte to inflammation in asthma has been extensively studied through descriptions of T cell subsets in the airway wall of asthmatic patients and from animal and cellular models. Allergy-driven airway disease is mediated primarily by the T helper (Th)2 cell subset. Other subsets, such as Th1, Th17, invariant natural killer T and CD8+ T cells likely contribute to the development, and possibly the progression of established disease. Resolution of inflammation is controlled in part by regulatory T cells. Therapies directed at T cells and their cytokines have been disappointing in asthma despite, in some instances, promising results on allergen challenge. This suggests that the induction of asthma may be T-cell-mediated and allergen-triggered, whereas disease may be sustained and exacerbated by other mechanisms.
哮喘是一种炎症性疾病，其与气道壁中活化的 T 细胞有关。通过描述哮喘患者气道壁中的 T 细胞亚群以及通过动物和细胞模型，已经广泛研究了 T 淋巴细胞对哮喘炎症的贡献。过敏原驱动的气道疾病主要由辅助性 T 细胞（Th）2 细胞亚群介导。其他亚群，如 Th1、Th17、固有自然杀伤 T 细胞和 CD8+T 细胞可能有助于疾病的发展，并且可能有助于已建立疾病的进展。炎症的消退部分受到调节性 T 细胞的控制。尽管在某些情况下过敏原挑战的结果令人鼓舞，但针对 T 细胞及其细胞因子的治疗在哮喘中令人失望。这表明哮喘的诱导可能是 T 细胞介导的和过敏原触发的，而疾病可能通过其他机制持续和加重。
