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组织驻留的 MAIT 细胞产生的 IL-17 在儿童肺炎中局部诱导。

IL-17 production by tissue-resident MAIT cells is locally induced in children with pneumonia.

机构信息

Department of Respiratory Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Centre, State Key Laboratory of Respiratory Diseases, Guangzhou Medical University, Guangzhou, Guangdong, China.

School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China.

出版信息

Mucosal Immunol. 2020 Sep;13(5):824-835. doi: 10.1038/s41385-020-0273-y. Epub 2020 Feb 28.

DOI:10.1038/s41385-020-0273-y
PMID:32112047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7434594/
Abstract

Community-acquired pneumonia (CAP) contributes substantially to morbidity and mortality in children under the age of 5 years. In examining bronchoalveolar lavages (BALs) of children with CAP, we found that interleukin-17 (IL-17) production was significantly increased in severe CAP. Immune profiling showed that mucosal-associated invariant T (MAIT) cells from the BALs, but not blood, of CAP patients actively produced IL-17 (MAIT17). Single-cell RNA-sequencing revealed that MAIT17 resided in a BAL-resident PLZFCD103 MAIT subset with high expression of hypoxia-inducible factor 1α (HIF-1α), reflecting the hypoxic state of the inflamed tissue. CAP BALs also contained a T-bet MAIT1 subset and a novel DDIT3 (DNA damage-inducible transcript 3-positive) MAIT subset with low expression of HIF1A. Furthermore, MAIT17 differed from T-helper type 17 (Th17) cells in the expression of genes related to tissue location, innateness, and cytotoxicity. Finally, we showed that BAL monocytes were hyper-inflammatory and elicited differentiation of MAIT17. Thus, tissue-resident MAIT17 cells are induced at the infected respiratory mucosa, likely influenced by inflammatory monocytes, and contribute to IL-17-mediated inflammation during CAP.

摘要

社区获得性肺炎（CAP）是导致 5 岁以下儿童发病和死亡的主要原因。在研究 CAP 患儿的支气管肺泡灌洗液（BAL）时，我们发现严重 CAP 患儿的白细胞介素-17（IL-17）产生明显增加。免疫分析显示，来自 CAP 患者 BAL 中的黏膜相关不变 T（MAIT）细胞，而不是血液中的 MAIT 细胞，积极产生 IL-17（MAIT17）。单细胞 RNA 测序显示，MAIT17 位于 BAL 驻留的 PLZFCD103 MAIT 亚群中，该亚群高表达低氧诱导因子 1α（HIF-1α），反映了炎症组织的缺氧状态。CAP BAL 中还包含一个 T 细胞因子 MAIT1 亚群和一个新型 DDIT3（DNA 损伤诱导转录 3 阳性）MAIT 亚群，其 HIF1A 表达较低。此外，MAIT17 在与组织定位、先天性和细胞毒性相关的基因表达上与辅助性 T 细胞 17（Th17）细胞不同。最后，我们表明 BAL 单核细胞表现出过度炎症反应，并引发 MAIT17 的分化。因此，组织驻留的 MAIT17 细胞在感染的呼吸道黏膜中被诱导产生，可能受到炎症性单核细胞的影响，并在 CAP 期间促进 IL-17 介导的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/ae6d1c8f4bf3/41385_2020_273_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/ae6d1c8f4bf3/41385_2020_273_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/4a220d0983f2/41385_2020_273_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/312508a7c3ad/41385_2020_273_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/e67f932cf061/41385_2020_273_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1515/7434594/ae6d1c8f4bf3/41385_2020_273_Fig5_HTML.jpg

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