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肺部感染与炎症中的自然杀伤细胞。

Natural killer cells in infection and inflammation of the lung.

作者信息

Culley Fiona J

机构信息

Respiratory Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London W21PG, UK.

出版信息

Immunology. 2009 Oct;128(2):151-63. doi: 10.1111/j.1365-2567.2009.03167.x.

DOI:10.1111/j.1365-2567.2009.03167.x
PMID:19740372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2767305/
Abstract

The lungs are a major site of entry of pathogens into the body and thus require rapid and effective innate responses to prevent pathogens establishing infection and to limit their spread. Additionally, the immune response in the lung must be tightly regulated such that pathogens are cleared, but immunopathology and chronic inflammation are prevented. In this review, I consider the role of natural killer (NK) cells in pulmonary infection and inflammation, specifically their contributions to influenza, tuberculosis, asthma and chronic obstructive pulmonary disease (COPD), which are major causes of morbidity and mortality world-wide. Despite evidence of the importance of NK cells in these diseases, there are still major gaps in our understanding of how their function is regulated in this unique tissue environment. Understanding how different beneficial and detrimental effector functions of NK cells are triggered will be crucial if NK cells are to be exploited therapeutically in respiratory disease.

摘要

肺是病原体进入人体的主要部位,因此需要快速有效的先天性免疫反应来防止病原体感染并限制其传播。此外,肺部的免疫反应必须受到严格调控,以便清除病原体,同时防止免疫病理和慢性炎症。在这篇综述中,我探讨了自然杀伤(NK)细胞在肺部感染和炎症中的作用,特别是它们在流感、肺结核、哮喘和慢性阻塞性肺疾病(COPD)中的作用,这些疾病是全球发病和死亡的主要原因。尽管有证据表明NK细胞在这些疾病中很重要,但我们对其在这种独特组织环境中的功能调控仍知之甚少。如果要在呼吸系统疾病中利用NK细胞进行治疗,了解NK细胞不同的有益和有害效应功能是如何触发的将至关重要。

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本文引用的文献

1
Interleukin-22-producing natural killer cells and lymphoid tissue inducer-like cells in mucosal immunity.黏膜免疫中产生白细胞介素-22的自然杀伤细胞和类淋巴组织诱导细胞
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Identification of MICA as a susceptibility gene for pulmonary Mycobacterium avium complex infection.鉴定MICA作为肺部鸟分枝杆菌复合群感染的易感基因。
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MICA polymorphisms and decreased expression of the MICA receptor NKG2D contribute to idiopathic pulmonary fibrosis susceptibility.MICA基因多态性及MICA受体NKG2D表达降低与特发性肺纤维化易感性相关。
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