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Molecular requirements involved in suppression of EAE by synthetic basic copolymers of amino acids.

作者信息

Webb C, Teitelbaum D, Herz A, Arnon R, Sela M

出版信息

Immunochemistry. 1976 Apr;13(4):333-7. doi: 10.1016/0019-2791(76)90344-x.

DOI:10.1016/0019-2791(76)90344-x
PMID:59690
Abstract
摘要

相似文献

1
Molecular requirements involved in suppression of EAE by synthetic basic copolymers of amino acids.
Immunochemistry. 1976 Apr;13(4):333-7. doi: 10.1016/0019-2791(76)90344-x.
2
Experimental allergic encephalomyelitis--susceptibility and suppression.实验性变应性脑脊髓炎——易感性与抑制作用
Immunol Rev. 1981;55:5-30. doi: 10.1111/j.1600-065x.1981.tb00337.x.
3
Protection against experimental allergic encephalomyelitis.
Nature. 1972 Dec 29;240(5383):564-6. doi: 10.1038/240564b0.
4
Experimental allergic encephalomyelitis (EAE).实验性变应性脑脊髓炎
Neurosci Res Program Bull. 1971 Sep;9(4):499-502.
5
Antigen-induced suppression of mitogen responses and resistance to experimental autoimmune encephalomyelitis.抗原诱导的丝裂原反应抑制及对实验性自身免疫性脑脊髓炎的抵抗力
Cell Immunol. 1983 May;78(1):43-55. doi: 10.1016/0008-8749(83)90258-7.
6
Selective blocking of voltage-gated K+ channels improves experimental autoimmune encephalomyelitis and inhibits T cell activation.电压门控钾通道的选择性阻断可改善实验性自身免疫性脑脊髓炎并抑制T细胞活化。
J Immunol. 2001 Jan 15;166(2):936-44. doi: 10.4049/jimmunol.166.2.936.
7
In vitro and in vivo immune responses to homologous myelin basic protein in experimental allergic encephalomyelitis.实验性变应性脑脊髓炎中对同源髓鞘碱性蛋白的体外和体内免疫反应
Cell Immunol. 1974 Mar 30;11(1-3):212-20. doi: 10.1016/0008-8749(74)90021-5.
8
Immune responses to myelin basic protein in mycobacterial-induced suppression of experimental allergic encephalomyelitis.分枝杆菌诱导的实验性变应性脑脊髓炎抑制中对髓鞘碱性蛋白的免疫反应
Cell Immunol. 1974 Nov;14(2):242-54. doi: 10.1016/0008-8749(74)90209-3.
9
Antigen-induced inhibition of experimental allergic encephalomyelitis. III. Localization of an inhibitory site distinct from the major encephalitogenic determinant of myelin basic protein.抗原诱导的实验性变应性脑脊髓炎抑制作用。III. 与髓鞘碱性蛋白主要致脑炎决定簇不同的抑制位点的定位
J Immunol. 1975 Jan;114(1 Pt 1):191-4.
10
In vivo and in vitro immunological cross-reactions between basic encephalitogen and synthetic basic polypeptides capable of suppressing experimental allergic encephalomyelitis.碱性脑（脊髓）炎原与能够抑制实验性变应性脑脊髓炎的合成碱性多肽之间的体内和体外免疫交叉反应。
Eur J Immunol. 1973 May;3(5):279-86. doi: 10.1002/eji.1830030506.

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B-Cell Activity Predicts Response to Glatiramer Acetate and Interferon in Relapsing-Remitting Multiple Sclerosis.B 细胞活性可预测复发缓解型多发性硬化症对格拉替雷和干扰素的应答。
Neurol Neuroimmunol Neuroinflamm. 2021 Mar 11;8(3). doi: 10.1212/NXI.0000000000000980. Print 2021 May.
2
Synthetic Cationic Autoantigen Mimics Glatiramer Acetate Persistence at the Site of Injection and Is Efficacious Against Experimental Autoimmune Encephalomyelitis.合成阳离子自身抗原模拟醋酸格拉替雷在注射部位的持久性，并对实验性自身免疫性脑脊髓炎有效。
Front Immunol. 2021 Jan 18;11:603029. doi: 10.3389/fimmu.2020.603029. eCollection 2020.
3
Glatiramer acetate persists at the injection site and draining lymph nodes via electrostatically-induced aggregation.
醋酸格拉替雷通过静电诱导聚集在注射部位和引流淋巴结中持续存在。
J Control Release. 2019 Jan 10;293:36-47. doi: 10.1016/j.jconrel.2018.11.007. Epub 2018 Nov 7.
4
Interferon beta and glatiramer acetate therapy.干扰素β和醋酸格拉替雷治疗。
Neurotherapeutics. 2013 Jan;10(1):2-18. doi: 10.1007/s13311-012-0163-4.
5
Glatiramer acetate in the treatment of multiple sclerosis: emerging concepts regarding its mechanism of action.醋酸格拉替雷治疗多发性硬化症：作用机制的新观点。
CNS Drugs. 2011 May;25(5):401-14. doi: 10.2165/11588120-000000000-00000.
6
Pathophysiology of multiple sclerosis.多发性硬化症的病理生理学
J Neurol. 2008 Dec;255 Suppl 6:2-6. doi: 10.1007/s00415-008-6001-2.
7
Mechanism of action of glatiramer acetate in treatment of multiple sclerosis.醋酸格拉替雷治疗多发性硬化症的作用机制。
Neurotherapeutics. 2007 Oct;4(4):647-53. doi: 10.1016/j.nurt.2007.08.002.
8
Therapeutic vaccines in autoimmunity.自身免疫性疾病中的治疗性疫苗
Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2(Suppl 2):14586-92. doi: 10.1073/pnas.0404826101. Epub 2004 Aug 12.
9
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.
10
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.