• 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

对实验性自身免疫性脑脊髓炎具有抗性的小鼠,其胸腺中髓鞘碱性蛋白的表达增加,且髓鞘碱性蛋白特异性T细胞耐受性增强。

Mice resistant to experimental autoimmune encephalomyelitis have increased thymic expression of myelin basic protein and increased MBP specific T cell tolerance.

作者信息

Liu H, MacKenzie-Graham A J, Kim S, Voskuhl R R

机构信息

UCLA Dept. of Neurology, 710 Westwood Plaza, Los Angeles, CA 90095, USA.

出版信息

J Neuroimmunol. 2001 Apr 2;115(1-2):118-26. doi: 10.1016/s0165-5728(01)00269-7.

DOI:10.1016/s0165-5728(01)00269-7
PMID:11282161
Abstract

The relationship between expression of the autoantigens in thymi and susceptibility to autoimmune disease was determined in the experimental autoimmune encephalomyelitis (EAE) model. In two different sets of MHC congenic strains of mice characterized by differential susceptibility to EAE, levels of expression of MBP were shown to be higher in the more resistant strain. These data raised the possibility that more central tolerance to MBP may occur in more resistant strains. Differential tolerance was then evidenced by a decrease in T cell responses to MBP 83-102 in the more resistant strains. Together, these data indicate that the list of non-MHC genes involved in susceptibility to autoimmune disease should include genes which regulate expression of autoantigens in thymi.

摘要

在实验性自身免疫性脑脊髓炎(EAE)模型中,确定了胸腺中自身抗原的表达与自身免疫性疾病易感性之间的关系。在两组对EAE易感性不同的MHC同基因小鼠品系中,髓鞘碱性蛋白(MBP)的表达水平在抗性更强的品系中更高。这些数据增加了在抗性更强的品系中可能对MBP产生更多中枢耐受的可能性。随后,在抗性更强的品系中,T细胞对MBP 83 - 102的反应降低,证明了存在差异耐受性。这些数据共同表明,参与自身免疫性疾病易感性的非MHC基因列表应包括调节胸腺中自身抗原表达的基因。

相似文献

1
Mice resistant to experimental autoimmune encephalomyelitis have increased thymic expression of myelin basic protein and increased MBP specific T cell tolerance.对实验性自身免疫性脑脊髓炎具有抗性的小鼠,其胸腺中髓鞘碱性蛋白的表达增加,且髓鞘碱性蛋白特异性T细胞耐受性增强。
J Neuroimmunol. 2001 Apr 2;115(1-2):118-26. doi: 10.1016/s0165-5728(01)00269-7.
2
Analysis of the T cell repertoire for myelin basic protein in thymus-grafted and other types of chimera: evidence that major histocompatibility complex molecules on accessory cells rather than T cell specificity mainly regulate susceptibility to autoimmune encephalomyelitis.胸腺移植嵌合体及其他类型嵌合体中针对髓鞘碱性蛋白的T细胞库分析:辅助细胞上的主要组织相容性复合体分子而非T细胞特异性主要调节自身免疫性脑脊髓炎易感性的证据
Eur J Immunol. 1990 Sep;20(9):2119-26. doi: 10.1002/eji.1830200934.
3
Acquired tolerance to experimental autoimmune encephalomyelitis by intrathymic injection of myelin basic protein or its major encephalitogenic peptide.通过胸腺内注射髓鞘碱性蛋白或其主要致脑炎肽获得对实验性自身免疫性脑脊髓炎的耐受性。
J Exp Med. 1993 Aug 1;178(2):559-66. doi: 10.1084/jem.178.2.559.
4
Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II.实验性自身免疫性脑脊髓炎抗性小鼠具有高度致脑炎性的髓鞘碱性蛋白(MBP)特异性T细胞克隆,这些克隆能以高亲和力识别与MHC II类分子结合的MBP肽段。
J Immunol. 1995 Jan 1;154(1):388-98.
5
Age-dependent T cell tolerance and autoimmunity to myelin basic protein.年龄依赖性T细胞对髓鞘碱性蛋白的耐受性和自身免疫性。
Immunity. 2001 Apr;14(4):471-81. doi: 10.1016/s1074-7613(01)00127-3.
6
Two minor determinants of myelin basic protein induce experimental allergic encephalomyelitis in SJL/J mice.髓鞘碱性蛋白的两个次要决定簇可在SJL/J小鼠中诱发实验性变应性脑脊髓炎。
J Exp Med. 1988 Jul 1;168(1):213-27. doi: 10.1084/jem.168.1.213.
7
Mechanisms of acquired thymic tolerance in experimental autoimmune encephalomyelitis: thymic dendritic-enriched cells induce specific peripheral T cell unresponsiveness in vivo.实验性自身免疫性脑脊髓炎中获得性胸腺耐受的机制:富含胸腺树突状细胞在体内诱导外周T细胞特异性无反应性。
J Exp Med. 1995 Aug 1;182(2):357-66. doi: 10.1084/jem.182.2.357.
8
Pathologic role and temporal appearance of newly emerging autoepitopes in relapsing experimental autoimmune encephalomyelitis.复发性实验性自身免疫性脑脊髓炎中新出现的自身表位的病理作用及时间表现
J Immunol. 2000 Jan 15;164(2):670-8. doi: 10.4049/jimmunol.164.2.670.
9
The major histocompatibility complex influences myelin basic protein 63-88-induced T cell cytokine profile and experimental autoimmune encephalomyelitis.主要组织相容性复合体影响髓鞘碱性蛋白63 - 88诱导的T细胞细胞因子谱及实验性自身免疫性脑脊髓炎。
Eur J Immunol. 1993 Dec;23(12):3089-95. doi: 10.1002/eji.1830231207.
10
Subtle effects on myelin basic protein-specific T cell responses can lead to a major reduction in disease susceptibility in experimental allergic encephalomyelitis.对髓鞘碱性蛋白特异性T细胞反应的细微影响可导致实验性变态反应性脑脊髓炎的疾病易感性大幅降低。
J Immunol. 2000 Jul 1;165(1):75-82. doi: 10.4049/jimmunol.165.1.75.

引用本文的文献

1
Type I interferons provide additive signals for murine regulatory B cell induction by Schistosoma mansoni eggs.I 型干扰素为曼氏血吸虫卵诱导的小鼠调节性 B 细胞提供附加信号。
Eur J Immunol. 2019 Aug;49(8):1226-1234. doi: 10.1002/eji.201847858. Epub 2019 May 29.
2
Down-regulation of Myelin Gene Expression in Human Oligodendrocytes by Nitric Oxide: Implications for Demyelination in Multiple Sclerosis.一氧化氮对人少突胶质细胞中髓鞘基因表达的下调作用:对多发性硬化症脱髓鞘的影响
J Clin Cell Immunol. 2013 Jul 31;4. doi: 10.4172/2155-9899.1000157.
3
Cholera toxin B subunit linked to glutamic acid decarboxylase suppresses dendritic cell maturation and function.
霍乱毒素 B 亚单位与谷氨酸脱羧酶偶联可抑制树突状细胞成熟和功能。
Vaccine. 2011 Oct 26;29(46):8451-8. doi: 10.1016/j.vaccine.2011.07.077. Epub 2011 Jul 30.
4
Suppression of dendritic cell activation by diabetes autoantigens linked to the cholera toxin B subunit.通过与霍乱毒素 B 亚单位相关的糖尿病自身抗原抑制树突状细胞的活化。
Immunobiology. 2011 Apr;216(4):447-56. doi: 10.1016/j.imbio.2010.09.008. Epub 2010 Sep 24.
5
Redox regulation of cytokine-mediated inhibition of myelin gene expression in human primary oligodendrocytes.细胞因子介导的人原代少突胶质细胞髓鞘基因表达抑制的氧化还原调节
Free Radic Biol Med. 2005 Sep 15;39(6):823-31. doi: 10.1016/j.freeradbiomed.2005.05.014.
6
Detection of thyroglobulin mRNA as truncated isoform(s) in mouse thymus.在小鼠胸腺中检测截短异构体形式的甲状腺球蛋白mRNA。
Immunology. 2005 May;115(1):85-9. doi: 10.1111/j.1365-2567.2005.02119.x.