Department of Allergy, Asthma and Clinical Immunology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, South Korea.
Clin Exp Immunol. 2010 Jul 1;161(1):159-70. doi: 10.1111/j.1365-2249.2010.04151.x. Epub 2010 Apr 29.
Natural killer T (NK T) cells have been shown to play an essential role in the development of allergen-induced airway hyperresponsiveness (AHR) and/or airway inflammation in mouse models of acute asthma. Recently, NK T cells have been reported to be required for the development of AHR in a virus induced chronic asthma model. We investigated whether NK T cells were required for the development of allergen-induced AHR, airway inflammation and airway remodelling in a mouse model of chronic asthma. CD1d-/- mice that lack NK T cells were used for the experiments. In the chronic model, AHR, eosinophilic inflammation, remodelling characteristics including mucus metaplasia, subepithelial fibrosis and increased mass of the airway smooth muscle, T helper type 2 (Th2) immune response and immunoglobulin (Ig)E production were equally increased in both CD1d-/- mice and wild-type mice. However, in the acute model, AHR, eosinophilic inflammation, Th2 immune response and IgE production were significantly decreased in the CD1d-/- mice compared to wild-type. CD1d-dependent NK T cells may not be required for the development of allergen-induced AHR, eosinophilic airway inflammation and airway remodelling in chronic asthma model, although they play a role in the development of AHR and eosinophilic inflammation in acute asthma model.
自然杀伤 T(NK T)细胞已被证明在变应原诱导的气道高反应性(AHR)和/或急性哮喘小鼠模型中的气道炎症发展中发挥重要作用。最近,据报道 NK T 细胞对于病毒诱导的慢性哮喘模型中 AHR 的发展是必需的。我们研究了 NK T 细胞是否是变应原诱导的 AHR、气道炎症和气道重塑发展所必需的,在慢性哮喘的小鼠模型中进行了实验。用于实验的 CD1d-/- 小鼠缺乏 NK T 细胞。在慢性模型中,AHR、嗜酸性粒细胞炎症、重塑特征包括粘液化生、上皮下纤维化和气道平滑肌质量增加、辅助性 T 细胞 2(Th2)免疫反应和免疫球蛋白(Ig)E 产生在 CD1d-/- 小鼠和野生型小鼠中均同等增加。然而,在急性模型中,与野生型相比,CD1d-/- 小鼠的 AHR、嗜酸性粒细胞炎症、Th2 免疫反应和 IgE 产生显著降低。虽然 CD1d 依赖性 NK T 细胞在急性哮喘模型中 AHR 和嗜酸性粒细胞炎症的发展中起作用,但它们可能不是变应原诱导的 AHR、嗜酸性粒细胞气道炎症和气道重塑发展所必需的,在慢性哮喘模型中。