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PTX 指导感染小鼠中肺驻留记忆 T 细胞的发育。

PTX Instructs the Development of Lung-Resident Memory T Cells in Infected Mice.

机构信息

Centre d'Immunologie de Marseille-Luminy (CIML), Aix-Marseille University, UM2, Institut National de la Santé et de la Recherche Médicale (INSERM), U1104, Centre National de la Recherche Scientifique (CNRS), UMR7280, Parc Scientifique et Technologique de Luminy, Case 906, 13288 Marseille, France.

Laboratoire Adhesion & Inflammation, UMR INSERM 1067, UMR CNRS 7333, Aix-Marseille Université Case 937, CEDEX 09, 13288 Marseille, France.

出版信息

Toxins (Basel). 2021 Sep 8;13(9):632. doi: 10.3390/toxins13090632.

DOI:10.3390/toxins13090632
PMID:34564636
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8470914/
Abstract

Whooping cough is a severe, highly contagious disease of the human respiratory tract, caused by . The pathogenicity requires several virulence factors, including toxin (PTX), a key component of current available vaccines. Current vaccines do not induce mucosal immunity. Tissue-resident memory T cells (Trm) are among the first lines of defense against invading pathogens and are involved in long-term protection. However, the factors involved in Trm establishment remain unknown. Comparing two strains expressing PTX (WT) or not (ΔPTX), we show that the toxin is required to generate both lung CD4 and CD8 Trm. Co-administering purified PTX with ΔPTX is sufficient to generate these Trm subsets. Importantly, adoptive transfer of lung CD4 or CD8 Trm conferred protection against in naïve mice. Taken together, our data demonstrate for the first time a critical role for PTX in the induction of mucosal long-term protection against .

摘要

百日咳是一种严重的、高度传染性的人类呼吸道疾病,由 引起。致病性需要几种毒力因子,包括 毒素 (PTX),这是当前可用疫苗的关键组成部分。目前的疫苗不能诱导黏膜免疫。组织驻留记忆 T 细胞 (Trm) 是抵御入侵病原体的第一道防线之一,参与长期保护。然而,参与 Trm 建立的因素尚不清楚。比较表达 PTX(WT)或不表达(ΔPTX)的两种 株,我们表明毒素是产生肺部 CD4 和 CD8 Trm 所必需的。同时给予纯化的 PTX 和 ΔPTX 足以产生这些 Trm 亚群。重要的是,肺 CD4 或 CD8 Trm 的过继转移赋予了对 感染的保护作用。总之,我们的数据首次证明了 PTX 在诱导针对 的黏膜长期保护中的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/5eae56eea789/toxins-13-00632-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/3f0bba0eae68/toxins-13-00632-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/e2a2f9920163/toxins-13-00632-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/bcf15cc49028/toxins-13-00632-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/c89ab365abd5/toxins-13-00632-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/5eae56eea789/toxins-13-00632-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/3f0bba0eae68/toxins-13-00632-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/e2a2f9920163/toxins-13-00632-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/bcf15cc49028/toxins-13-00632-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/c89ab365abd5/toxins-13-00632-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68cc/8470914/5eae56eea789/toxins-13-00632-g005.jpg

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本文引用的文献

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Location, location, location: Tissue resident memory T cells in mice and humans.位置,位置,位置:小鼠和人类组织驻留记忆 T 细胞。
Sci Immunol. 2019 Apr 5;4(34). doi: 10.1126/sciimmunol.aas9673.
2
Immunization with whole cell but not acellular pertussis vaccines primes CD4 T cells that sustain protective immunity against nasal colonization with Bordetella pertussis.全细胞而非无细胞百日咳疫苗免疫可诱导 CD4 T 细胞,维持对百日咳博德特氏菌鼻定植的保护性免疫。
Emerg Microbes Infect. 2019;8(1):169-185. doi: 10.1080/22221751.2018.1564630.
3
Intravital mucosal imaging of CD8 resident memory T cells shows tissue-autonomous recall responses that amplify secondary memory.
活体内黏膜成像显示 CD8 记忆 T 细胞具有组织自主的记忆应答反应,可扩增次级记忆。
Nat Immunol. 2018 Feb;19(2):173-182. doi: 10.1038/s41590-017-0029-3. Epub 2018 Jan 8.
4
An update of the global burden of pertussis in children younger than 5 years: a modelling study.全球 5 岁以下儿童百日咳负担的更新:一项建模研究。
Lancet Infect Dis. 2017 Sep;17(9):974-980. doi: 10.1016/S1473-3099(17)30390-0. Epub 2017 Jun 13.
5
Lung CD4 Tissue-Resident Memory T Cells Mediate Adaptive Immunity Induced by Previous Infection of Mice with .肺CD4组织驻留记忆T细胞介导小鼠先前感染……所诱导的适应性免疫。 (原文中“with”后面内容缺失)
J Immunol. 2017 Jul 1;199(1):233-243. doi: 10.4049/jimmunol.1602051. Epub 2017 May 22.
6
Tissue resident memory T cells and viral immunity.组织驻留记忆性T细胞与病毒免疫
Curr Opin Virol. 2017 Feb;22:44-50. doi: 10.1016/j.coviro.2016.11.011. Epub 2016 Dec 14.
7
Transcriptional Regulation of Tissue-Resident Lymphocytes.组织驻留淋巴细胞的转录调控。
Trends Immunol. 2017 Feb;38(2):94-103. doi: 10.1016/j.it.2016.11.004. Epub 2016 Dec 9.
8
IL-17-Producing Innate and Pathogen-Specific Tissue Resident Memory γδ T Cells Expand in the Lungs of Bordetella pertussis-Infected Mice.产生白细胞介素-17的先天性和病原体特异性组织驻留记忆γδT细胞在百日咳博德特氏菌感染小鼠的肺部中扩增。
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9
Programs for the persistence, vigilance and control of human CD8 lung-resident memory T cells.用于持久、警戒和控制人类 CD8 肺驻留记忆 T 细胞的方案。
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