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自然杀伤 T 细胞在慢性哮喘小鼠模型中过敏原诱导的气道高反应性、炎症和重塑的发展中是可有可无的。

Natural killer T cells are dispensable in the development of allergen-induced airway hyperresponsiveness, inflammation and remodelling in a mouse model of chronic asthma.

机构信息

Department of Allergy, Asthma and Clinical Immunology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, South Korea.

出版信息

Clin Exp Immunol. 2010 Jul 1;161(1):159-70. doi: 10.1111/j.1365-2249.2010.04151.x. Epub 2010 Apr 29.

DOI:10.1111/j.1365-2249.2010.04151.x
PMID:20456411
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2940161/
Abstract

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.

摘要

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。

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本文引用的文献

1
CD4+ cells are required for chronic eosinophilic lung inflammation but not airway remodeling.慢性嗜酸性粒细胞性肺部炎症需要CD4+细胞,但气道重塑则不需要。
Am J Physiol Lung Cell Mol Physiol. 2009 Feb;296(2):L229-35. doi: 10.1152/ajplung.90543.2008. Epub 2008 Dec 5.
2
Activation of nonclassical CD1d-restricted NK T cells induces airway hyperreactivity in beta 2-microglobulin-deficient mice.非经典CD1d限制性自然杀伤T细胞的激活在β2-微球蛋白缺陷小鼠中诱导气道高反应性。
J Immunol. 2008 Oct 1;181(7):4560-4569. doi: 10.4049/jimmunol.181.7.4560.
3
New insights into airway remodelling in asthma and its possible modulation.哮喘气道重塑及其可能调节的新见解。
Curr Opin Allergy Clin Immunol. 2008 Oct;8(5):367-75. doi: 10.1097/ACI.0b013e32830a7086.
4
Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models.哮喘中的气道高反应性:来自体外模型系统和动物模型的经验教训。
Eur Respir J. 2008 Aug;32(2):487-502. doi: 10.1183/09031936.00023608.
5
Airway hyperresponsiveness is dissociated from airway wall structural remodeling.气道高反应性与气道壁结构重塑无关。
J Allergy Clin Immunol. 2008 Aug;122(2):335-41, 341.e1-3. doi: 10.1016/j.jaci.2008.05.020. Epub 2008 Jun 24.
6
Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.先天性免疫反应的持续激活会将呼吸道病毒感染转化为慢性肺病。
Nat Med. 2008 Jun;14(6):633-40. doi: 10.1038/nm1770. Epub 2008 May 18.
7
Administration of IL-33 induces airway hyperresponsiveness and goblet cell hyperplasia in the lungs in the absence of adaptive immune system.在缺乏适应性免疫系统的情况下,给予白细胞介素-33可诱导肺部气道高反应性和杯状细胞增生。
Int Immunol. 2008 Jun;20(6):791-800. doi: 10.1093/intimm/dxn037. Epub 2008 Apr 29.
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Ozone exposure in a mouse model induces airway hyperreactivity that requires the presence of natural killer T cells and IL-17.在小鼠模型中暴露于臭氧会诱发气道高反应性,这需要自然杀伤T细胞和白细胞介素-17的存在。
J Exp Med. 2008 Feb 18;205(2):385-93. doi: 10.1084/jem.20071507. Epub 2008 Feb 4.
9
Epithelium dysfunction in asthma.哮喘中的上皮功能障碍。
J Allergy Clin Immunol. 2007 Dec;120(6):1233-44; quiz 1245-6. doi: 10.1016/j.jaci.2007.10.025.
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Time sequence of airway remodeling in a mouse model of chronic asthma: the relation with airway hyperresponsiveness.慢性哮喘小鼠模型中气道重塑的时间序列:与气道高反应性的关系
J Korean Med Sci. 2007 Apr;22(2):183-91. doi: 10.3346/jkms.2007.22.2.183.