• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

同源单纯疱疹病毒1型(HSV1)和α-突触核蛋白肽可刺激帕金森病患者的T细胞反应。

Homologous HSV1 and alpha-synuclein peptides stimulate a T cell response in Parkinson's disease.

作者信息

Caggiu E, Paulus K, Galleri G, Arru G, Manetti R, Sechi G P, Sechi L A

机构信息

Dipartimento di Scienze Biomediche, Sezione di Microbiologia, Università di Sassari, Italy.

Dipartimento di Medicina Clinica e Sperimentale, Università di Sassari, Viale San Pietro 43b, 07100 Sassari, Italy.

出版信息

J Neuroimmunol. 2017 Sep 15;310:26-31. doi: 10.1016/j.jneuroim.2017.06.004. Epub 2017 Jun 15.

DOI:10.1016/j.jneuroim.2017.06.004
PMID:28778441
Abstract

Environmental factors are implicated in the development of Parkinson's disease (PD). The aim of this study is to investigate the role of cell-mediated immunity upon a specific immune-stimulation with HSV-1 and human alpha-synuclein homologues peptides by using the intracellular cytokine method on Parkinson's patients and healthy controls. The study showed, for the first time, a specific response to TNF-α CD8, CD4 and NK cells after stimulation in PD patients. Our data show a possible role of the immune system in the pathogenesis of Parkinson's disease, and that HSV-1 infections may lead to a progression of the disease.

摘要

环境因素与帕金森病(PD)的发病有关。本研究旨在通过细胞内细胞因子法,对帕金森病患者和健康对照者进行单纯疱疹病毒1型(HSV-1)和人α-突触核蛋白同源肽特异性免疫刺激后,研究细胞介导免疫的作用。该研究首次显示,帕金森病患者在刺激后,TNF-α、CD8、CD4和NK细胞出现特异性反应。我们的数据表明免疫系统在帕金森病发病机制中可能发挥作用,且HSV-1感染可能导致疾病进展。

相似文献

1
Homologous HSV1 and alpha-synuclein peptides stimulate a T cell response in Parkinson's disease.同源单纯疱疹病毒1型(HSV1)和α-突触核蛋白肽可刺激帕金森病患者的T细胞反应。
J Neuroimmunol. 2017 Sep 15;310:26-31. doi: 10.1016/j.jneuroim.2017.06.004. Epub 2017 Jun 15.
2
Humoral cross reactivity between α-synuclein and herpes simplex-1 epitope in Parkinson's disease, a triggering role in the disease?帕金森病中α-突触核蛋白与单纯疱疹病毒1型表位之间的体液交叉反应性:在该疾病中起触发作用?
J Neuroimmunol. 2016 Feb 15;291:110-4. doi: 10.1016/j.jneuroim.2016.01.007. Epub 2016 Jan 9.
3
T cells from patients with Parkinson's disease recognize α-synuclein peptides.帕金森病患者的T细胞可识别α-突触核蛋白肽段。
Nature. 2017 Jun 29;546(7660):656-661. doi: 10.1038/nature22815. Epub 2017 Jun 21.
4
Immune responses to oligomeric α-synuclein in Parkinson's disease peripheral blood mononuclear cells.帕金森病患者外周血单个核细胞中寡聚化α-突触核蛋白的免疫反应。
J Neurol. 2024 Sep;271(9):5916-5929. doi: 10.1007/s00415-024-12554-3. Epub 2024 Jul 10.
5
CD4 T cells mediate brain inflammation and neurodegeneration in a mouse model of Parkinson's disease.CD4 T 细胞在帕金森病小鼠模型中介导脑部炎症和神经退行性变。
Brain. 2021 Aug 17;144(7):2047-2059. doi: 10.1093/brain/awab103.
6
Autoimmunity in Parkinson's Disease: The Role of α-Synuclein-Specific T Cells.帕金森病中的自身免疫:α-突触核蛋白特异性 T 细胞的作用。
Front Immunol. 2019 Feb 25;10:303. doi: 10.3389/fimmu.2019.00303. eCollection 2019.
7
Natural killer cells of Parkinson's disease patients are set up for activation: a possible role for innate immunity in the pathogenesis of this disease.帕金森病患者的自然杀伤细胞处于激活状态:固有免疫在该疾病发病机制中的潜在作用。
Parkinsonism Relat Disord. 2008;14(1):46-51. doi: 10.1016/j.parkreldis.2007.05.013. Epub 2007 Aug 16.
8
A possible role for humoral immunity in the pathogenesis of Parkinson's disease.体液免疫在帕金森病发病机制中的可能作用。
Brain. 2005 Nov;128(Pt 11):2665-74. doi: 10.1093/brain/awh625. Epub 2005 Oct 11.
9
Alpha-synuclein triggers T-cell response. Is Parkinson's disease an autoimmune disorder?α-突触核蛋白引发T细胞反应。帕金森病是一种自身免疫性疾病吗?
Mov Disord. 2017 Sep;32(9):1327. doi: 10.1002/mds.27116. Epub 2017 Aug 7.
10
Alpha-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's disease.在帕金森病早期,α-突触核蛋白重新分布至黑质中的神经黑素脂质。
Brain. 2005 Nov;128(Pt 11):2654-64. doi: 10.1093/brain/awh584. Epub 2005 Jul 6.

引用本文的文献

1
Human pegivirus alters brain and blood immune and transcriptomic profiles of patients with Parkinson's disease.人佩吉病毒改变帕金森病患者的大脑和血液免疫及转录组特征。
JCI Insight. 2025 Jul 8;10(13). doi: 10.1172/jci.insight.189988.
2
Peripheral immune cell response to stimulation stratifies Parkinson's disease progression from prodromal to clinical stages.外周免疫细胞对刺激的反应将帕金森病从前驱期到临床期的进展进行分层。
Commun Biol. 2025 May 8;8(1):716. doi: 10.1038/s42003-025-08088-7.
3
Peripheral immune cell response to stimulation stratifies Parkinson's disease progression from prodromal to clinical stages.
外周免疫细胞对刺激的反应将帕金森病从前驱期到临床期的进展进行分层。
bioRxiv. 2024 Dec 7:2024.12.05.625499. doi: 10.1101/2024.12.05.625499.
4
From Gut Microbiomes to Infectious Pathogens: Neurological Disease Game Changers.从肠道微生物群到感染性病原体:改变神经疾病的因素
Mol Neurobiol. 2025 Jan;62(1):1184-1204. doi: 10.1007/s12035-024-04323-0. Epub 2024 Jul 5.
5
Systemic immune challenge exacerbates neurodegeneration in a model of neurological lysosomal disease.系统性免疫挑战加重神经溶酶体疾病模型中的神经退行性变。
EMBO Mol Med. 2024 Jul;16(7):1579-1602. doi: 10.1038/s44321-024-00092-4. Epub 2024 Jun 18.
6
Experimental Models to Study Immune Dysfunction in the Pathogenesis of Parkinson's Disease.用于研究帕金森病发病机制中免疫功能障碍的实验模型
Int J Mol Sci. 2024 Apr 14;25(8):4330. doi: 10.3390/ijms25084330.
7
Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.神经亲和性病毒感染与神经退行性疾病:自噬途径的潜在作用。
CNS Neurosci Ther. 2024 Jun;30(6):e14548. doi: 10.1111/cns.14548. Epub 2023 Dec 11.
8
The role of immune cells in the course of Parkinson's disease.免疫细胞在帕金森病病程中的作用。
Ibrain. 2021 Jun 28;7(2):146-151. doi: 10.1002/j.2769-2795.2021.tb00077.x. eCollection 2021 Jun.
9
Microglia Mediated Neuroinflammation in Parkinson's Disease.小胶质细胞介导的帕金森病神经炎症。
Cells. 2023 Mar 25;12(7):1012. doi: 10.3390/cells12071012.
10
Antibodies against HSV-1 and Curli Show the Highest Correlation in Parkinson's Disease Patients in Comparison to Healthy Controls.与健康对照组相比,抗 HSV-1 和 Curli 抗体在帕金森病患者中相关性最高。
Int J Mol Sci. 2022 Nov 26;23(23):14816. doi: 10.3390/ijms232314816.