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Oral tolerance with copolymer 1 for the treatment of multiple sclerosis.

作者信息

Weiner H L

出版信息

Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3333-5. doi: 10.1073/pnas.96.7.3333.

DOI:10.1073/pnas.96.7.3333
PMID:10097037
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC34268/
Abstract
摘要

相似文献

1
Oral tolerance with copolymer 1 for the treatment of multiple sclerosis.用共聚物1进行口服耐受治疗多发性硬化症。
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3333-5. doi: 10.1073/pnas.96.7.3333.
2
Glatiramer acetate (Copaxone) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosis.醋酸格拉替雷(考帕松)可诱导多发性硬化症患者产生退化性、Th2极化免疫反应。
J Clin Invest. 2000 Apr;105(7):967-76. doi: 10.1172/JCI8970.
3
Recent insights into the mechanism of action of glatiramer acetate.对醋酸格拉替雷作用机制的最新认识。
J Neuroimmunol. 2011 Jun;235(1-2):9-17. doi: 10.1016/j.jneuroim.2011.01.009. Epub 2011 Mar 13.
4
The use of glatiramer acetate in the treatment of multiple sclerosis.醋酸格拉替雷在多发性硬化症治疗中的应用。
Adv Neurol. 2006;98:273-92.
5
Glatiramer acetate (Copaxone) therapy for multiple sclerosis.醋酸格拉替雷(考帕松)治疗多发性硬化症。
Pharmacol Ther. 2003 May;98(2):245-55. doi: 10.1016/s0163-7258(03)00036-6.
6
Characterization of T cell lines derived from glatiramer-acetate-treated multiple sclerosis patients.源自醋酸格拉替雷治疗的多发性硬化症患者的T细胞系的特征分析
J Neuroimmunol. 2000 Aug 1;108(1-2):201-6. doi: 10.1016/s0165-5728(00)00263-0.
7
Glatiramer: a second look. With longer follow-up: still no proven benefit in multiple sclerosis.格拉替雷:再审视。随着随访时间延长:对多发性硬化症仍无已证实的益处。
Prescrire Int. 2009 Dec;18(104):252.
8
Immunomodulation of experimental autoimmune encephalomyelitis by oral administration of copolymer 1.口服共聚物1对实验性自身免疫性脑脊髓炎的免疫调节作用
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3842-7. doi: 10.1073/pnas.96.7.3842.
9
Glatiramer acetate in the treatment of multiple sclerosis.醋酸格拉替雷治疗多发性硬化症
Expert Opin Pharmacother. 2001 Jul;2(7):1149-65. doi: 10.1517/14656566.2.7.1149.
10
Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability. Copolymer 1 Multiple Sclerosis Study Group.醋酸格拉替雷(考帕松)的长期使用耐受性良好,并能维持其对多发性硬化症复发率和残疾程度的临床疗效。共聚物1多发性硬化症研究组。
Neurology. 1998 Mar;50(3):701-8. doi: 10.1212/wnl.50.3.701.

引用本文的文献

1
Glatiramer acetate attenuates the activation of CD4 T cells by modulating STAT1 and -3 signaling in glia.醋酸格拉替雷通过调节神经胶质细胞中 STAT1 和 -3 信号转导来抑制 CD4 T 细胞的激活。
Sci Rep. 2017 Jan 17;7:40484. doi: 10.1038/srep40484.
2
Induction of mucosal tolerance in SLE: a sniff or a sip away from ameliorating lupus?系统性红斑狼疮中黏膜耐受的诱导:通过嗅闻或啜饮就能改善狼疮吗?
Clin Immunol. 2009 Feb;130(2):111-22. doi: 10.1016/j.clim.2008.08.028. Epub 2008 Oct 19.
3
Autoimmune concepts of multiple sclerosis as a basis for selective immunotherapy: from pipe dreams to (therapeutic) pipelines.作为选择性免疫治疗基础的多发性硬化症自身免疫概念:从白日梦到(治疗)途径。
Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2(Suppl 2):14599-606. doi: 10.1073/pnas.0404874101. Epub 2004 Aug 11.
4
Oral tolerance.口服耐受
Immunol Res. 2003;28(3):265-84. doi: 10.1385/IR:28:3:265.
5
Beneficial effect of co-polymer 1 on cytokine production by CD4 T cells in multiple sclerosis.共聚物1对多发性硬化症中CD4 T细胞细胞因子产生的有益作用。
Immunology. 2001 Dec;104(4):383-91. doi: 10.1046/j.1365-2567.2001.01322.x.
6
CD40L in autoimmunity and mucosally induced tolerance.自身免疫和黏膜诱导耐受中的CD40L
J Clin Invest. 2002 Jan;109(2):171-3. doi: 10.1172/JCI14930.
7
Risk-benefit assessment of glatiramer acetate in multiple sclerosis.醋酸格拉替雷治疗多发性硬化症的风险效益评估。
Drug Saf. 2001;24(13):979-90. doi: 10.2165/00002018-200124130-00005.
8
Oral tolerance, an active immunologic process mediated by multiple mechanisms.口服耐受,一种由多种机制介导的主动免疫过程。
J Clin Invest. 2000 Oct;106(8):935-7. doi: 10.1172/JCI11348.
9
Multiple sclerosis: comparison of copolymer-1- reactive T cell lines from treated and untreated subjects reveals cytokine shift from T helper 1 to T helper 2 cells.多发性硬化症:来自接受治疗和未接受治疗受试者的共聚物-1反应性T细胞系的比较显示细胞因子从辅助性T1细胞向辅助性T2细胞转变。
Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7452-7. doi: 10.1073/pnas.97.13.7452.
10
Induction of oral tolerance to the acetylcholine receptor for treatment of myasthenia gravis.诱导对乙酰胆碱受体的口服耐受以治疗重症肌无力。
J Clin Invest. 1999 Dec;104(12):1667-8. doi: 10.1172/JCI8775.

本文引用的文献

1
Oral tolerance: mechanisms and therapeutic applications.口服耐受:机制与治疗应用
Adv Immunol. 1999;73:153-264. doi: 10.1016/s0065-2776(08)60787-7.
2
Oral administration of myelin basic protein is superior to myelin in suppressing established relapsing experimental autoimmune encephalomyelitis.口服髓鞘碱性蛋白在抑制已建立的复发型实验性自身免疫性脑脊髓炎方面优于髓磷脂。
J Immunol. 1999 May 15;162(10):6247-54.
3
Immunomodulation of experimental autoimmune encephalomyelitis by oral administration of copolymer 1.口服共聚物1对实验性自身免疫性脑脊髓炎的免疫调节作用
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3842-7. doi: 10.1073/pnas.96.7.3842.
4
Treatment of multiple sclerosis with copolymer-1 (Copaxone): implicating mechanisms of Th1 to Th2/Th3 immune-deviation.用共聚肽-1(考帕松)治疗多发性硬化症:涉及Th1向Th2/Th3免疫偏移的机制
J Neuroimmunol. 1998 Dec 1;92(1-2):113-21. doi: 10.1016/s0165-5728(98)00191-x.
5
Control of immune pathology by regulatory T cells.调节性T细胞对免疫病理的控制。
Curr Opin Immunol. 1998 Dec;10(6):649-55. doi: 10.1016/s0952-7915(98)80084-8.
6
Copolymer 1 acts against the immunodominant epitope 82-100 of myelin basic protein by T cell receptor antagonism in addition to major histocompatibility complex blocking.共聚体1除了阻断主要组织相容性复合体外,还通过T细胞受体拮抗作用对抗髓鞘碱性蛋白的免疫显性表位82 - 100。
Proc Natl Acad Sci U S A. 1999 Jan 19;96(2):634-9. doi: 10.1073/pnas.96.2.634.
7
Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1.由共聚物1诱导的Th2型T细胞系和克隆对实验性自身免疫性脑脊髓炎的旁观者抑制作用
J Neuroimmunol. 1998 Nov 2;91(1-2):135-46. doi: 10.1016/s0165-5728(98)00166-0.
8
A critical role for transforming growth factor-beta in donor transfusion-induced allograft tolerance.转化生长因子-β在供体输血诱导的同种异体移植耐受中的关键作用。
J Clin Invest. 1998 Dec 1;102(11):1920-6. doi: 10.1172/JCI4221.
9
Synthetic amino acid copolymers that bind to HLA-DR proteins and inhibit type II collagen-reactive T cell clones.与HLA-DR蛋白结合并抑制II型胶原反应性T细胞克隆的合成氨基酸共聚物。
Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12528-31. doi: 10.1073/pnas.95.21.12528.
10
IL-10 is critical in the regulation of autoimmune encephalomyelitis as demonstrated by studies of IL-10- and IL-4-deficient and transgenic mice.白细胞介素-10在自身免疫性脑脊髓炎的调节中起关键作用,白细胞介素-10和白细胞介素-4缺陷及转基因小鼠的研究已证明了这一点。
J Immunol. 1998 Oct 1;161(7):3299-306.