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Antibodies specific for VB8 receptor peptide suppress experimental autoimmune encephalomyelitis.

作者信息

Hashim G A, Vandenbark A A, Galang A B, Diamanduros T, Carvalho E, Srinivasan J, Jones R, Vainiene M, Morrison W J, Offner H

机构信息

Department of Microbiology, St. Luke's-Roosevelt Hospital, New York, NY 10025.

出版信息

J Immunol. 1990 Jun 15;144(12):4621-7.

PMID:1693637
Abstract

Recent studies from our laboratory have shown, for the first time, that a synthetic peptide from that TCR VB chain used preferentially by encephalitogenic T cells induced the formation of protective, MHC class I-restricted T cells and prevented the development of EAE in Lewis rats. In this report we 1) demonstrate that immunization with the TCR-VB8-39-59 peptide generated peptide-specific antibodies that protect against experimental autoimmune encephalomyelitis induced by either of the two distinct encephalitogenic epitopes of basic protein, and 2) characterize the production and biologic functions of rat and rabbit antibody responses to the TCR peptide. The antibodies in both species increased in titer over time, were highly specific for the immunogen by direct reaction and inhibition assays, stained only VB8+ T cells, and suppressed clinical signs and to lesser extent the number of histologic lesions of experimental autoimmune encephalomyelitis mediated by VB8+ T cells. Coupled with our previous work, these results indicate that both humoral and cellular responses to the TCR-VB8-39-59 peptide can contribute independent immunoregulatory effects on encephalitogenic T lymphocytes that use common V region genes in response to epitopes of myelin basic protein.

摘要

相似文献

1
Antibodies specific for VB8 receptor peptide suppress experimental autoimmune encephalomyelitis.
J Immunol. 1990 Jun 15;144(12):4621-7.
2
Characterization of the immune response to a secondary encephalitogenic epitope of basic protein in Lewis rats. I. T cell receptor peptide regulation of T cell clones expressing cross-reactive V beta genes.对Lewis大鼠碱性蛋白的继发性致脑炎表位的免疫反应特征。I. 表达交叉反应性Vβ基因的T细胞克隆的T细胞受体肽调节
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3
Coculture of TCR peptide-specific T cells with basic protein-specific T cells inhibits proliferation, IL-3 mRNA, and transfer of experimental autoimmune encephalomyelitis.TCR肽特异性T细胞与碱性蛋白特异性T细胞共培养可抑制实验性自身免疫性脑脊髓炎的增殖、白细胞介素-3信使核糖核酸及转移。
J Immunol. 1994 Dec 1;153(11):4988-96.
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A cross-reactive idiotope on T cells from PL/J mice and Lewis rats that recognizes different myelin basic protein encephalitogenic epitopes but is restricted by TCR V beta 8.2.来自PL/J小鼠和Lewis大鼠的T细胞上的一种交叉反应性独特型决定簇,其识别不同的髓鞘碱性蛋白致脑炎表位,但受TCR Vβ8.2限制。
J Immunol. 1994 Sep 1;153(5):2340-51.
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Preferential distribution of V beta 8.2-positive T cells in the central nervous system of rats with myelin basic protein-induced autoimmune encephalomyelitis.髓鞘碱性蛋白诱导的自身免疫性脑脊髓炎大鼠中枢神经系统中Vβ8.2阳性T细胞的优先分布。
Eur J Immunol. 1993 Oct;23(10):2399-406. doi: 10.1002/eji.1830231004.
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Spontaneous development of protective anti-T cell receptor autoimmunity targeted against a natural EAE-regulatory idiotope located within the 39-59 region of the TCR-V beta 8.2 chain.
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Diverse T cell receptor beta chain usage by rat encephalitogenic T cells reactive to residues 68-88 of myelin basic protein.对髓鞘碱性蛋白68 - 88位残基产生反应的大鼠致脑炎性T细胞对T细胞受体β链的多样使用情况
Eur J Immunol. 1993 Feb;23(2):494-8. doi: 10.1002/eji.1830230229.
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Immunization with a synthetic T-cell receptor V-region peptide protects against experimental autoimmune encephalomyelitis.用合成的T细胞受体V区肽进行免疫可预防实验性自身免疫性脑脊髓炎。
Nature. 1989 Oct 12;341(6242):541-4. doi: 10.1038/341541a0.
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T cell lines specific for an immunodominant epitope of human basic protein define an encephalitogenic determinant for experimental autoimmune encephalomyelitis-resistant LOU/M rats.针对人碱性蛋白免疫显性表位的T细胞系确定了实验性自身免疫性脑脊髓炎抗性LOU/M大鼠的致脑炎决定簇。
J Immunol. 1991 Jan 15;146(2):515-20.
10
Determinants of human myelin basic protein that induce encephalitogenic T cells in Lewis rats.在Lewis大鼠中诱导致脑炎性T细胞的人髓鞘碱性蛋白的决定因素。
J Immunol. 1989 Dec 1;143(11):3512-6.

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