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排泄分泌抗原对仔猪TGF-β信号通路及Th17细胞分化的影响:蛋白质组学分析

Effects of Excretory-Secretory Antigens on the TGF-β Signaling Pathway and Th17 Cell Differentiation in Piglets, a Proteomic Analysis.

作者信息

He Wei, Mu Qianqian, Li Lizhu, Sun Xiaoqing, Fan Xianmin, Yang Fengjiao, Liu Meichen, Zhou Biying

机构信息

Department of Parasitology, Zunyi Medical University, Zunyi 563000, China.

出版信息

Microorganisms. 2023 Feb 27;11(3):601. doi: 10.3390/microorganisms11030601.

DOI:10.3390/microorganisms11030601
PMID:36985175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10056668/
Abstract

Excretory-secretory antigens (ESAs) of can directly regulate the proliferation and differentiation of host T regulatory (Treg) cells, thus inhibiting host immune responses. However, previous studies have only focused on this phenomenon, and the molecular mechanisms behind the ways in which ESAs regulate the differentiation of host Treg/Th17 cells have not been reported. We collected CD3 T cells stimulated by ESAs through magnetic bead sorting and used label-free quantification (LFQ) proteomics techniques to analyze the signaling pathways of ESAs regulating Treg/Th17 cell differentiation. Through gene set enrichment analysis (GSEA), we found that ESAs could upregulate the TGF-β signaling pathway and downregulate Th17 cell differentiation in piglet T cells. Interestingly, we also found that the IL-2/STAT5 signaling pathway also affects the downregulation of Th17 cell differentiation. ESAs activate the TGF-β signaling pathway and the IL-2/STAT5 signaling pathway in host T cells to further regulate the differentiation of Treg/Th17 cells in order to evade host immune attack. This study lays the foundation for the subsequent verification of these pathways, and further clarifies the molecular mechanism of -mediated immune evasion.

摘要

[某种生物]的排泄分泌抗原(ESAs)可直接调节宿主调节性T(Treg)细胞的增殖和分化,从而抑制宿主免疫反应。然而,以往的研究仅关注这一现象,而ESAs调节宿主Treg/Th17细胞分化的分子机制尚未见报道。我们通过磁珠分选收集了受ESAs刺激的CD3 T细胞,并使用无标记定量(LFQ)蛋白质组学技术分析ESAs调节Treg/Th17细胞分化的信号通路。通过基因集富集分析(GSEA),我们发现ESAs可上调仔猪T细胞中的TGF-β信号通路并下调Th17细胞分化。有趣的是,我们还发现IL-2/STAT5信号通路也影响Th17细胞分化的下调。ESAs激活宿主T细胞中的TGF-β信号通路和IL-2/STAT5信号通路,以进一步调节Treg/Th17细胞的分化,从而逃避宿主免疫攻击。本研究为后续这些通路的验证奠定了基础,并进一步阐明了[某种生物]介导的免疫逃避的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/84c92703f9aa/microorganisms-11-00601-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/729d2ed6dd75/microorganisms-11-00601-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/3f68c288d453/microorganisms-11-00601-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/6a2b6fbb1280/microorganisms-11-00601-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/a920c4ac7580/microorganisms-11-00601-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/84c92703f9aa/microorganisms-11-00601-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/729d2ed6dd75/microorganisms-11-00601-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/3f68c288d453/microorganisms-11-00601-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/6a2b6fbb1280/microorganisms-11-00601-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/a920c4ac7580/microorganisms-11-00601-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8817/10056668/84c92703f9aa/microorganisms-11-00601-g005.jpg

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本文引用的文献

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Activation of primary hepatic stellate cells and liver fibrosis induced by targeting TGF-β1/Smad signaling in schistosomiasis in mice.靶向 TGF-β1/Smad 信号通路在小鼠血吸虫病中诱导的原代肝星状细胞激活和肝纤维化。
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Regulation of piglet T-cell immune responses by thioredoxin peroxidase from excretory-secretory antigens.
排泄分泌抗原中的硫氧还蛋白过氧化物酶对仔猪T细胞免疫反应的调节
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