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IL-9 命运报告基因揭示了在肺部炎症中先天 IL-9 反应的诱导。

An IL-9 fate reporter demonstrates the induction of an innate IL-9 response in lung inflammation.

机构信息

Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, Mill Hill, UK.

出版信息

Nat Immunol. 2011 Oct 9;12(11):1071-7. doi: 10.1038/ni.2133.

DOI:10.1038/ni.2133
PMID:21983833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3198843/
Abstract

Interleukin 9 (IL-9) is a cytokine linked to lung inflammation, but its cellular origin and function remain unclear. Here we describe a reporter mouse strain designed to map the fate of cells that have activated IL-9. We found that during papain-induced lung inflammation, IL-9 production was largely restricted to innate lymphoid cells (ILCs). IL-9 production by ILCs depended on IL-2 from adaptive immune cells and was rapidly lost in favor of other cytokines, such as IL-13 and IL-5. Blockade of IL-9 production via neutralizing antibodies resulted in much lower expression of IL-13 and IL-5, which suggested that ILCs provide the missing link between the well-established functions of IL-9 in the regulation of type 2 helper T cell cytokines and responses.

摘要

白细胞介素 9(IL-9)是一种与肺部炎症相关的细胞因子,但它的细胞起源和功能仍不清楚。在这里,我们描述了一种报告小鼠品系,用于绘制已经激活白细胞介素 9 的细胞的命运图。我们发现,在木瓜蛋白酶诱导的肺部炎症中,白细胞介素 9 的产生主要局限于固有淋巴细胞(ILC)。ILC 产生白细胞介素 9 依赖于适应性免疫细胞的 IL-2,并迅速被其他细胞因子(如白细胞介素 13 和白细胞介素 5)取代。通过中和抗体阻断白细胞介素 9 的产生导致白细胞介素 13 和白细胞介素 5 的表达水平降低很多,这表明 ILC 提供了在调节 2 型辅助 T 细胞细胞因子和反应方面 IL-9 功能的缺失环节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/64a49a521870/ukmss-36406-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/ddb0749a25b6/ukmss-36406-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/167edc2544ec/ukmss-36406-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/4d6353972557/ukmss-36406-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/3a56a85856cf/ukmss-36406-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/35e40129c22d/ukmss-36406-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/b6ad645b71b0/ukmss-36406-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/64a49a521870/ukmss-36406-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/ddb0749a25b6/ukmss-36406-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/167edc2544ec/ukmss-36406-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/4d6353972557/ukmss-36406-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/3a56a85856cf/ukmss-36406-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/35e40129c22d/ukmss-36406-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/b6ad645b71b0/ukmss-36406-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9619/3198843/64a49a521870/ukmss-36406-f0007.jpg

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