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不同物种对髓系来源抑制细胞的差异性调控

Differential Regulation of Myeloid-Derived Suppressor Cells by Species.

作者信息

Singh Anurag, Lelis Felipe, Braig Stefanie, Schäfer Iris, Hartl Dominik, Rieber Nikolaus

机构信息

University Children's Hospital and Interdisciplinary Center for Infectious Diseases, University of Tübingen Tübingen, Germany.

University Children's Hospital and Interdisciplinary Center for Infectious Diseases, University of TübingenTübingen, Germany; Department of Pediatrics, Kinderklinik München Schwabing, StKM GmbH und Klinikum rechts der Isar, Technische Universität MünchenMunich, Germany.

出版信息

Front Microbiol. 2016 Oct 13;7:1624. doi: 10.3389/fmicb.2016.01624. eCollection 2016.

DOI:10.3389/fmicb.2016.01624
PMID:27790210
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5061774/
Abstract

Myeloid-derived suppressor cells (MDSCs) are innate immune cells characterized by their ability to suppress T-cell responses. Recently, we demonstrated that the human-pathogenic fungi and induced a distinct subset of neutrophilic MDSCs. To dissect -mediated MDSC induction in more depth, we studied the relative efficacy of different pathogenic non- species to induce and functionally modulate neutrophilic MDSCs, including , and . Our data demonstrate that the extent of MDSC generation is largely dependent on the species with MDSCs induced by and showing a higher suppressive activity compared to MDSCs induced by In summary, these studies show that fungal MDSC induction is differentially regulated at the species level and differentially affects effector T-cell responses.

摘要

髓系来源的抑制细胞(MDSCs)是一类固有免疫细胞,其特征在于具有抑制T细胞反应的能力。最近,我们证明了人类致病真菌和诱导了嗜中性MDSCs的一个独特亚群。为了更深入地剖析介导的MDSC诱导作用,我们研究了不同致病性非物种诱导和功能调节嗜中性MDSCs的相对效力,包括、和。我们的数据表明,MDSC生成的程度在很大程度上取决于物种,与诱导的MDSCs相比,由和诱导的MDSCs表现出更高的抑制活性。总之,这些研究表明,真菌MDSC诱导在物种水平上受到差异调节,并对效应T细胞反应产生不同影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/a95447f3a6e4/fmicb-07-01624-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/91e6626e13af/fmicb-07-01624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/b3475021e363/fmicb-07-01624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/9aac1225fedf/fmicb-07-01624-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/a95447f3a6e4/fmicb-07-01624-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/91e6626e13af/fmicb-07-01624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/b3475021e363/fmicb-07-01624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/9aac1225fedf/fmicb-07-01624-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48b3/5061774/a95447f3a6e4/fmicb-07-01624-g004.jpg

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Epigenetic targeting of myeloid-derived suppressor cells: time to move into infectious diseases?
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