脂肪酸代谢在营养不良和蠕虫感染期间ILC2介导的屏障保护中的关键作用。
Critical role of fatty acid metabolism in ILC2-mediated barrier protection during malnutrition and helminth infection.
作者信息
Wilhelm Christoph, Harrison Oliver J, Schmitt Vanessa, Pelletier Martin, Spencer Sean P, Urban Joseph F, Ploch Michelle, Ramalingam Thirumalai R, Siegel Richard M, Belkaid Yasmine
机构信息
Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Institute of Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, University of Bonn, 53127 Bonn, Germany
Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
出版信息
J Exp Med. 2016 Jul 25;213(8):1409-18. doi: 10.1084/jem.20151448. Epub 2016 Jul 18.
Innate lymphoid cells (ILC) play an important role in many immune processes, including control of infections, inflammation, and tissue repair. To date, little is known about the metabolism of ILC and whether these cells can metabolically adapt in response to environmental signals. Here we show that type 2 innate lymphoid cells (ILC2), important mediators of barrier immunity, predominantly depend on fatty acid (FA) metabolism during helminth infection. Further, in situations where an essential nutrient, such as vitamin A, is limited, ILC2 sustain their function and selectively maintain interleukin 13 (IL-13) production via increased acquisition and utilization of FA. Together, these results reveal that ILC2 preferentially use FAs to maintain their function in the context of helminth infection or malnutrition and propose that enhanced FA usage and FA-dependent IL-13 production by ILC2 could represent a host adaptation to maintain barrier immunity under dietary restriction.
固有淋巴细胞（ILC）在许多免疫过程中发挥重要作用，包括控制感染、炎症和组织修复。迄今为止，对于ILC的代谢以及这些细胞是否能够根据环境信号进行代谢适应了解甚少。在此我们表明，2型固有淋巴细胞（ILC2）作为屏障免疫的重要介质，在蠕虫感染期间主要依赖脂肪酸（FA）代谢。此外，在诸如维生素A等必需营养素受限的情况下，ILC2通过增加FA的获取和利用来维持其功能并选择性地维持白细胞介素13（IL-13）的产生。这些结果共同表明，在蠕虫感染或营养不良的情况下，ILC2优先利用FA来维持其功能，并提出ILC2增强的FA利用和FA依赖性IL-13产生可能代表宿主在饮食限制下维持屏障免疫的一种适应性反应。
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