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从小鼠肺中分离第2组固有淋巴细胞

Isolation of Group 2 Innate Lymphoid Cells from Mouse Lungs.

作者信息

Duerr Claudia U, Fritz Jörg H

机构信息

Department of Microbiology and Immunology, McGill University Research Centre on Complex Traits (MRCCT), McGill University, 3649 Promenade-Sir-William Osler, Bellini Pavilion Room 371, Montreal, QC, Canada, H3G 0B1.

Department of Physiology, McGill University Research Centre on Complex Traits (MRCCT), McGill University, 3649 Promenade-Sir-William Osler, Bellini Pavilion Room 371, Montreal, QC, Canada, H3G 0B1.

出版信息

Methods Mol Biol. 2017;1656:253-261. doi: 10.1007/978-1-4939-7237-1_16.

DOI:10.1007/978-1-4939-7237-1_16
PMID:28808975
Abstract

The recently described group 2 innate lymphoid cells (ILC2) exert critical roles in type 2 immune responses, epithelial repair at mucosal tissues and metabolic homeostasis. ILC2 release large amounts of type 2 cytokines such as interleukin 4 (IL-4), IL-5, and IL-13, driving type 2 immunity such as the defense against helminths. However, if not tightly regulated ILC2 can trigger unwanted type 2 immunopathologies including allergic airway inflammation, airway hyper-responsiveness, and atopic dermatitis. Viral respiratory tract infections, archetypal triggers of type 1 immune responses, often give rise to pulmonary type 2 immunopathologies such as asthma and asthma exacerbations. Interestingly, pulmonary viral infections induce the release of IL-33, followed by induction of ILC2-mediated pulmonary type 2 immunopathology independent of the adaptive immune system. Due to their scarcity at steady state but also after infection and inflammation, pulmonary ILC2 are challenging to work with. In this chapter, we describe the detection and isolation procedure of pulmonary mouse ILC2 by flow cytometry and compare four distinct enzymatic mouse lung tissue processing protocols for optimized cell yield.

摘要

最近描述的2型固有淋巴细胞(ILC2)在2型免疫反应、粘膜组织的上皮修复和代谢稳态中发挥着关键作用。ILC2释放大量2型细胞因子,如白细胞介素4(IL-4)、IL-5和IL-13,驱动2型免疫,如对蠕虫的防御。然而,如果不进行严格调控,ILC2会引发不必要的2型免疫病理,包括过敏性气道炎症、气道高反应性和特应性皮炎。病毒性呼吸道感染是1型免疫反应的典型触发因素,常常引发肺部2型免疫病理,如哮喘和哮喘加重。有趣的是,肺部病毒感染会诱导IL-33的释放,随后诱导ILC2介导的肺部2型免疫病理,且不依赖于适应性免疫系统。由于它们在稳态下以及感染和炎症后数量稀少,肺部ILC2难以进行研究。在本章中,我们描述了通过流式细胞术检测和分离肺部小鼠ILC2的程序,并比较了四种不同的酶促小鼠肺组织处理方案,以优化细胞产量。

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Regulation of group 2 innate lymphoid cells.2型固有淋巴细胞的调节
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