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本文引用的文献

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Long-term follow-up of EBV-positive lymphoproliferative disorders in a patient with systemic lupus erythematosus.系统性红斑狼疮患者EB病毒阳性淋巴增殖性疾病的长期随访
Med Mol Morphol. 2011 Dec;44(4):237-41. doi: 10.1007/s00795-011-0551-6. Epub 2011 Dec 17.
2
Exhausted cytotoxic control of Epstein-Barr virus in human lupus.人类狼疮中 EB 病毒的细胞毒性控制耗竭。
PLoS Pathog. 2011 Oct;7(10):e1002328. doi: 10.1371/journal.ppat.1002328. Epub 2011 Oct 20.
3
Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease. Epstein-Barr 病毒潜伏期的表观遗传失调与自身免疫性疾病的发生。
Adv Exp Med Biol. 2011;711:82-102. doi: 10.1007/978-1-4419-8216-2_7.
4
Secondary neuropsychiatric manifestations caused by Epstein-Barr virus encephalitis in a new onset systemic lupus erythematosus patient.继发于新发系统性红斑狼疮患者的 EBV 脑炎所致的神经精神性表现。
Rheumatol Int. 2012 Aug;32(8):2321-3. doi: 10.1007/s00296-011-1877-z. Epub 2011 May 24.
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Identification of novel microRNA signatures linked to human lupus disease activity and pathogenesis: miR-21 regulates aberrant T cell responses through regulation of PDCD4 expression.鉴定与人类狼疮疾病活动和发病机制相关的新型 microRNA 特征:miR-21 通过调节 PDCD4 表达来调节异常的 T 细胞反应。
Ann Rheum Dis. 2011 Aug;70(8):1496-506. doi: 10.1136/ard.2010.139857. Epub 2011 May 20.
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The genetics of systemic lupus erythematosus and implications for targeted therapy.系统性红斑狼疮的遗传学及其对靶向治疗的影响。
Ann Rheum Dis. 2011 Mar;70 Suppl 1:i37-43. doi: 10.1136/ard.2010.138057.
7
Molecular mechanisms of TNFR-associated factor 6 (TRAF6) utilization by the oncogenic viral mimic of CD40, latent membrane protein 1 (LMP1).肿瘤病毒模拟物 CD40 的潜伏膜蛋白 1(LMP1)利用肿瘤坏死因子受体相关因子 6(TRAF6)的分子机制。
J Biol Chem. 2011 Mar 25;286(12):9948-55. doi: 10.1074/jbc.M110.185983. Epub 2011 Jan 24.
8
Antibodies elicited in response to EBNA-1 may cross-react with dsDNA.针对 EBNA-1 产生的抗体可能与 dsDNA 发生交叉反应。
PLoS One. 2011 Jan 4;6(1):e14488. doi: 10.1371/journal.pone.0014488.
9
Simultaneous presentation of hemophagocytic syndrome and mesenteric vasculitis in a patient with systemic lupus erythematosus.系统性红斑狼疮患者同时出现噬血细胞综合征和肠系膜血管炎。
Mod Rheumatol. 2011 Jun;21(3):330-3. doi: 10.1007/s10165-010-0401-8. Epub 2011 Jan 13.
10
Genetic susceptibility to systemic lupus erythematosus in the genomic era.基因组时代系统性红斑狼疮的遗传易感性。
Nat Rev Rheumatol. 2010 Dec;6(12):683-92. doi: 10.1038/nrrheum.2010.176. Epub 2010 Nov 9.

狼疮与 EBV(爱泼斯坦-巴尔病毒)。

Lupus and Epstein-Barr.

机构信息

Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.

出版信息

Curr Opin Rheumatol. 2012 Jul;24(4):383-8. doi: 10.1097/BOR.0b013e3283535801.

DOI:10.1097/BOR.0b013e3283535801
PMID:22504579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3562348/
Abstract

PURPOSE OF REVIEW

Systemic lupus erythematosus (SLE) is a heterogeneous human disease influenced by a complex interplay of necessary, but not individually sufficient, factors. Although many genetic and environmental factors are associated with SLE, this review will focus on the evolving evidence for key Epstein-Barr virus (EBV)-specific roles in SLE, focusing on new experimental studies published during 2009, 2010, and 2011.

RECENT FINDINGS

SLE patients have a dysregulated immune response against EBV. EBV antigens exhibit structural molecular mimicry with common SLE antigens and functional molecular mimicry with critical immune-regulatory components. SLE patients, from a number of unique geographic regions, are shown to have higher rates of EBV seroconversion, especially against early EBV antigens, suggesting frequent viral reactivation. SLE patients also have increased EBV viral loads and impaired EBV-specific CD8 cytotoxic T cells, with impaired cytokine responses to EBV in lupus patients. Irregular cytokine production in plasmacytoid dendritic cells and CD69 CD4 T cells after stimulation with EBV has also been demonstrated.

SUMMARY

Recent advances demonstrate SLE-specific serologic responses, gene expression, viral load, T-cell responses, humoral fine specificity, and molecular mimicry with EBV, further supporting potential roles for EBV in lupus etiology and pathogenesis.

摘要

目的综述

系统性红斑狼疮(SLE)是一种异质性人类疾病,受多种必要但非单独充分的因素相互作用的影响。尽管许多遗传和环境因素与 SLE 相关,但本篇综述将重点关注 2009 年、2010 年和 2011 年期间发表的新实验研究中,关于 EBV 特异性在 SLE 中关键作用的不断发展的证据。

最新发现

SLE 患者存在针对 EBV 的失调免疫反应。EBV 抗原与常见的 SLE 抗原具有结构分子模拟性,与关键免疫调节成分具有功能分子模拟性。来自多个独特地理区域的 SLE 患者显示 EBV 血清转化率更高,尤其是针对早期 EBV 抗原,提示频繁的病毒再激活。SLE 患者还具有更高的 EBV 病毒载量和受损的 EBV 特异性 CD8 细胞毒性 T 细胞,对狼疮患者的 EBV 反应存在受损的细胞因子应答。此外,还已经证明在受到 EBV 刺激后,浆细胞样树突状细胞和 CD69+CD4+T 细胞中的不规则细胞因子产生。

总结

最近的进展表明了 SLE 特异性的血清学反应、基因表达、病毒载量、T 细胞反应、体液精细特异性和 EBV 分子模拟性,进一步支持 EBV 在狼疮病因和发病机制中的潜在作用。