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1
Enhanced susceptibility of T lymphocytes to oxidative stress in the absence of the cellular prion protein.在缺乏细胞朊蛋白的情况下，T淋巴细胞对氧化应激的易感性增强。
Cell Mol Life Sci. 2011 Feb;68(4):687-96. doi: 10.1007/s00018-010-0477-5. Epub 2010 Aug 18.
2
Prion protein-deficient neurons reveal lower glutathione reductase activity and increased susceptibility to hydrogen peroxide toxicity.朊病毒蛋白缺陷型神经元表现出较低的谷胱甘肽还原酶活性，并且对过氧化氢毒性的易感性增加。
Am J Pathol. 1999 Nov;155(5):1723-30. doi: 10.1016/S0002-9440(10)65487-9.
3
The octarepeat region of prion protein, but not the TM1 domain, is important for the antioxidant effect of prion protein.朊病毒蛋白的八肽重复区域而非跨膜结构域1，对朊病毒蛋白的抗氧化作用很重要。
Free Radic Biol Med. 2008 Dec 15;45(12):1622-30. doi: 10.1016/j.freeradbiomed.2008.08.024. Epub 2008 Sep 9.
4
PrP mutants with different numbers of octarepeat sequences are more susceptible to the oxidative stress.具有不同八肽重复序列数量的朊蛋白（PrP）突变体对氧化应激更敏感。
Sci China C Life Sci. 2008 Jul;51(7):630-9. doi: 10.1007/s11427-008-0062-4. Epub 2008 Jul 13.
5
Normal cellular prion protein protects against manganese-induced oxidative stress and apoptotic cell death.正常细胞朊蛋白可抵御锰诱导的氧化应激和凋亡性细胞死亡。
Toxicol Sci. 2007 Aug;98(2):495-509. doi: 10.1093/toxsci/kfm099. Epub 2007 May 4.
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Cellular prion protein modulates the intracellular calcium response to hydrogen peroxide.细胞朊蛋白调节细胞内对过氧化氢的钙反应。
J Neurochem. 2007 Jan;100(2):358-67. doi: 10.1111/j.1471-4159.2006.04256.x.
7
Prion protein regulates glutathione metabolism and neural glutamate and cysteine uptake via excitatory amino acid transporter 3.朊病毒蛋白通过兴奋性氨基酸转运体3调节谷胱甘肽代谢以及神经谷氨酸和半胱氨酸的摄取。
J Neurochem. 2015 May;133(4):558-71. doi: 10.1111/jnc.13071. Epub 2015 Mar 17.
8
Reactive oxygen species-mediated beta-cleavage of the prion protein in the cellular response to oxidative stress.活性氧介导的朊病毒蛋白β-切割在细胞对氧化应激的反应中
J Biol Chem. 2005 Oct 28;280(43):35914-21. doi: 10.1074/jbc.M507327200. Epub 2005 Aug 24.
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Reactive oxygen species (ROS)-mediated beta-cleavage of the prion protein in the mechanism of the cellular response to oxidative stress.活性氧（ROS）介导的朊病毒蛋白β-切割在细胞对氧化应激反应机制中的作用
Biochem Soc Trans. 2005 Nov;33(Pt 5):1123-5. doi: 10.1042/BST20051123.
10
Acute exposure to prion infection induces transient oxidative stress progressing to be cumulatively deleterious with chronic propagation in vitro.急性朊病毒感染会引发短暂的氧化应激，这种应激在体外的慢性传播过程中会逐渐累积，造成损害。
Free Radic Biol Med. 2011 Aug 1;51(3):594-608. doi: 10.1016/j.freeradbiomed.2011.03.035. Epub 2011 Apr 3.

引用本文的文献

1
Stress Resilience of Spermatozoa and Blood Mononuclear Cells without Prion Protein.不含朊病毒蛋白的精子和血液单核细胞的应激恢复力
Front Mol Biosci. 2018 Jan 24;5:1. doi: 10.3389/fmolb.2018.00001. eCollection 2018.
2
Deoxycytidine kinase augments ATM-Mediated DNA repair and contributes to radiation resistance.脱氧胞苷激酶增强ATM介导的DNA修复并有助于辐射抗性。
PLoS One. 2014 Aug 7;9(8):e104125. doi: 10.1371/journal.pone.0104125. eCollection 2014.
3
Gene expression resulting from PrPC ablation and PrPC overexpression in murine and cellular models.在小鼠和细胞模型中，由朊蛋白（PrPC）缺失和朊蛋白过表达所导致的基因表达。
Mol Neurobiol. 2014 Feb;49(1):413-23. doi: 10.1007/s12035-013-8529-0. Epub 2013 Aug 16.
4
Molecular responses of mouse macrophages to copper and copper oxide nanoparticles inferred from proteomic analyses.从蛋白质组学分析推断小鼠巨噬细胞对铜和氧化铜纳米粒子的分子反应。
Mol Cell Proteomics. 2013 Nov;12(11):3108-22. doi: 10.1074/mcp.M113.030742. Epub 2013 Jul 23.
5
Ablation of the cellular prion protein, PrPC, specifically on follicular dendritic cells has no effect on their maturation or function.细胞朊病毒蛋白（PrPC）的消融，特别是在滤泡树突状细胞上，对其成熟或功能没有影响。
Immunology. 2013 Mar;138(3):246-57. doi: 10.1111/imm.12031.
6
Trafficking of PrPc to mitochondrial raft-like microdomains during cell apoptosis.细胞凋亡过程中朊蛋白向线粒体筏样微域的转运。
Prion. 2012 Sep-Oct;6(4):354-8. doi: 10.4161/pri.20479. Epub 2012 Jul 30.
7
Recruitment of cellular prion protein to mitochondrial raft-like microdomains contributes to apoptosis execution.细胞朊蛋白向线粒体筏状微域的募集有助于细胞凋亡的执行。
Mol Biol Cell. 2011 Dec;22(24):4842-53. doi: 10.1091/mbc.E11-04-0348. Epub 2011 Oct 26.
8
Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding.朊蛋白（PrPC）通过调节 GluR6/7-PSD-95 结合对 JNK3 激活的作用对抗红藻氨酸诱导的癫痫发作和细胞死亡具有神经保护作用。
Mol Biol Cell. 2011 Sep;22(17):3041-54. doi: 10.1091/mbc.E11-04-0321. Epub 2011 Jul 14.

本文引用的文献

1
Oxidation of cofilin mediates T cell hyporesponsiveness under oxidative stress conditions.肌动蛋白结合蛋白的氧化介导氧化应激条件下T细胞低反应性。
Immunity. 2008 Sep 19;29(3):404-13. doi: 10.1016/j.immuni.2008.06.016. Epub 2008 Sep 4.
2
The prion's elusive reason for being.朊病毒存在的难以捉摸的原因。
Annu Rev Neurosci. 2008;31:439-77. doi: 10.1146/annurev.neuro.31.060407.125620.
3
Prion proteins: physiological functions and role in neurological disorders.朊病毒蛋白：生理功能及在神经疾病中的作用
J Neurol Sci. 2008 Jan 15;264(1-2):1-8. doi: 10.1016/j.jns.2007.06.019. Epub 2007 Aug 17.
4
The role of the cellular prion protein in the immune system.细胞朊蛋白在免疫系统中的作用。
Clin Exp Immunol. 2006 Oct;146(1):1-8. doi: 10.1111/j.1365-2249.2006.03194.x.
5
Functional implication of cellular prion protein in antigen-driven interactions between T cells and dendritic cells.细胞朊蛋白在T细胞与树突状细胞之间抗原驱动相互作用中的功能意义。
J Immunol. 2006 Jun 15;176(12):7254-62. doi: 10.4049/jimmunol.176.12.7254.
6
Early thymic T cell development in young transgenic mice overexpressing human Cu/Zn superoxide dismutase, a model of Down syndrome.年轻的过表达人铜锌超氧化物歧化酶的转基因小鼠的早期胸腺T细胞发育，一种唐氏综合征模型。
Free Radic Biol Med. 2006 Jun 1;40(11):1971-80. doi: 10.1016/j.freeradbiomed.2006.01.029. Epub 2006 Feb 21.
7
Overexpression of cellular prion protein induces an antioxidant environment altering T cell development in the thymus.细胞朊蛋白的过表达诱导了一种抗氧化环境，改变了胸腺中T细胞的发育。
J Immunol. 2006 Mar 15;176(6):3490-7. doi: 10.4049/jimmunol.176.6.3490.
8
PrPc capping in T cells promotes its association with the lipid raft proteins reggie-1 and reggie-2 and leads to signal transduction.T细胞中的朊蛋白（PrPc）加帽促进其与脂筏蛋白reggie-1和reggie-2的结合，并导致信号转导。
FASEB J. 2004 Nov;18(14):1731-3. doi: 10.1096/fj.04-2150fje. Epub 2004 Sep 2.
9
Reactive oxygen species induced by the deletion of peroxiredoxin II (PrxII) increases the number of thymocytes resulting in the enlargement of PrxII-null thymus.由过氧化物酶II（PrxII）缺失诱导产生的活性氧会增加胸腺细胞数量，导致PrxII基因敲除小鼠的胸腺增大。
Eur J Immunol. 2004 Aug;34(8):2119-28. doi: 10.1002/eji.200424962.
10
PrP(C) association with lipid rafts in the early secretory pathway stabilizes its cellular conformation.在早期分泌途径中，朊蛋白（C）与脂筏的结合稳定了其细胞构象。
Mol Biol Cell. 2004 Sep;15(9):4031-42. doi: 10.1091/mbc.e03-05-0271. Epub 2004 Jun 30.

在缺乏细胞朊蛋白的情况下，T淋巴细胞对氧化应激的易感性增强。

Enhanced susceptibility of T lymphocytes to oxidative stress in the absence of the cellular prion protein.

作者信息

Aude-Garcia Catherine, Villiers Christian, Candéias Serge M, Garrel Catherine, Bertrand Caroline, Collin Véronique, Marche Patrice N, Jouvin-Marche Evelyne

机构信息

CEA, DSV, iRTSV, Laboratoire Biochimie et Biophysique des Systèmes Intégrés, 17 rue des Martyrs, 38054, Grenoble Cedex 9, France.

出版信息

Cell Mol Life Sci. 2011 Feb;68(4):687-96. doi: 10.1007/s00018-010-0477-5. Epub 2010 Aug 18.

DOI:10.1007/s00018-010-0477-5
PMID:20717837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11114857/
Abstract

The cellular prion glycoprotein (PrP(C)) is ubiquitously expressed but its physiologic functions remain enigmatic, particularly in the immune system. Here, we demonstrate in vitro and in vivo that PrP(C) is involved in T lymphocytes response to oxidative stress. By monitoring the intracellular level of reduced glutathione, we show that PrP(-/-) thymocytes display a higher susceptibility to H(2)O(2) exposure than PrP(+/+) cells. Furthermore, we find that in mice fed with a restricted diet, a regimen known to increase the intracellular level of ROS, PrP(-/-) thymocytes are more sensitive to oxidative stress. PrP(C) function appears to be specific for oxidative stress, since no significant differences are observed between PrP(-/-) and PrP(+/+) mice exposed to other kinds of stress. We also show a marked evolution of the redox status of T cells throughout differentiation in the thymus. Taken together, our results clearly ascribe to PrP(C) a protective function in thymocytes against oxidative stress.

摘要

细胞朊蛋白糖蛋白（PrP(C)）在全身广泛表达，但其生理功能仍不清楚，尤其是在免疫系统中。在此，我们在体外和体内证明PrP(C)参与T淋巴细胞对氧化应激的反应。通过监测细胞内还原型谷胱甘肽水平，我们发现PrP(-/-)胸腺细胞比PrP(+/+)细胞对H(2)O(2)暴露更敏感。此外，我们发现，在喂食限制饮食（一种已知可增加细胞内活性氧水平的饮食方案）的小鼠中，PrP(-/-)胸腺细胞对氧化应激更敏感。PrP(C)的功能似乎对氧化应激具有特异性，因为在暴露于其他类型应激的PrP(-/-)和PrP(+/+)小鼠之间未观察到显著差异。我们还显示了胸腺中T细胞在整个分化过程中氧化还原状态的显著变化。综上所述，我们的结果清楚地表明PrP(C)在胸腺细胞中对氧化应激具有保护作用。