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几丁质酶样蛋白在杀灭线虫和宿主损伤之间的权衡中促进了白细胞介素 17 介导的嗜中性粒细胞增多。

Chitinase-like proteins promote IL-17-mediated neutrophilia in a tradeoff between nematode killing and host damage.

机构信息

Institute of Immunology and Infection Research, Centre for Immunity Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.

Department of Respiratory, Inflammation &Autoimmunity, MedImmune, Gaithersburg, Maryland, USA.

出版信息

Nat Immunol. 2014 Dec;15(12):1116-25. doi: 10.1038/ni.3023. Epub 2014 Oct 19.

DOI:10.1038/ni.3023
PMID:25326751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4338525/
Abstract

Enzymatically inactive chitinase-like proteins (CLPs) such as BRP-39, Ym1 and Ym2 are established markers of immune activation and pathology, yet their functions are essentially unknown. We found that Ym1 and Ym2 induced the accumulation of neutrophils through the expansion of γδ T cell populations that produced interleukin 17 (IL-17). While BRP-39 did not influence neutrophilia, it was required for IL-17 production in γδ T cells, which suggested that regulation of IL-17 is an inherent feature of mouse CLPs. Analysis of a nematode infection model, in which the parasite migrates through the lungs, revealed that the IL-17 and neutrophilic inflammation induced by Ym1 limited parasite survival but at the cost of enhanced lung injury. Our studies describe effector functions of CLPs consistent with innate host defense traits of the chitinase family.

摘要

酶失活的几丁质酶样蛋白（CLPs），如 BRP-39、Ym1 和 Ym2，是免疫激活和病理的既定标志物，但它们的功能本质上是未知的。我们发现 Ym1 和 Ym2 通过产生白细胞介素 17（IL-17）的 γδ T 细胞群体的扩增诱导中性粒细胞的积累。虽然 BRP-39 不影响中性粒细胞增多，但它是 γδ T 细胞中 IL-17 产生所必需的，这表明 IL-17 的调节是小鼠 CLPs 的固有特征。对一种线虫感染模型的分析表明，寄生虫通过肺部迁移，Ym1 诱导的 IL-17 和中性粒细胞炎症限制了寄生虫的存活，但代价是增强了肺部损伤。我们的研究描述了 CLPs 的效应功能，与几丁质酶家族的先天宿主防御特征一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/fd840c9187f1/emss-60525-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/1b98885afa99/emss-60525-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/7f36a737c7af/emss-60525-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/848b499dcf44/emss-60525-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/fd840c9187f1/emss-60525-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/1b98885afa99/emss-60525-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/58937a716251/emss-60525-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/2027d6b529ea/emss-60525-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/142b3af8fbaa/emss-60525-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/7a20f994a5a6/emss-60525-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/7f36a737c7af/emss-60525-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/848b499dcf44/emss-60525-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8766/4338525/fd840c9187f1/emss-60525-f0008.jpg

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