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Natural immunodominant and experimental autoimmune encephalomyelitis-protective determinants within the Lewis rat V beta 8.2 sequence include CDR2 and framework 3 idiotopes.

作者信息

Vainiene M, Celnik B, Vandenbark A A, Hashim G A, Offner H

机构信息

Neuroimmunology Research, Veterans Affairs Medical Center, Portland, OR 97201, USA.

出版信息

J Neurosci Res. 1996 Jan 15;43(2):137-45. doi: 10.1002/(SICI)1097-4547(19960115)43:2<137::AID-JNR2>3.0.CO;2-H.

DOI:10.1002/(SICI)1097-4547(19960115)43:2<137::AID-JNR2>3.0.CO;2-H
PMID:8820962
Abstract

The V beta 8.2-39-59 peptide has served as a prototypic natural regulatory idiotope in Lewis rats developing experimental autoimmune encephalomyelitis (EAE). The purpose of the present study was to determine if additional regulatory regions were contained within the V beta 8.2 sequence expressed by most encephalogenic T cells. A comprehensive strategy utilizing V beta 8+ hybridomas, a recombinant (r) V beta 8.2 molecule, and overlapping synthetic V beta 8.2 peptides reconfirmed the natural recognition of the 39-59 idiotope, and revealed a second immunodominant and EAE-protective determinant residing within residues 71-90. Both the V beta 8.2-39-59 and V beta 8.2-71-90 peptides were immunogenic, and each was recognized after immunization of Lewis rats with V beta 8+ cells or rV beta 8.2, indicating the preservation of these epitopes during the processing of the V beta 8.2 chain. Moreover, both epitopes were recognized naturally by T cells from rats developing or recovering from EAE that had never been purposefully immunized with V beta 8.2 peptides or rV beta 8.2. Of additional interest, the V beta 8.2-31-50 peptide was recognized by T cells from some rats immunized with complete Freund's adjuvant (CFA) alone. This peptide possessed mildly protective activity against EAE and thus could account for sporadic reports of CFA interference in EAE.

摘要

相似文献

1
Natural immunodominant and experimental autoimmune encephalomyelitis-protective determinants within the Lewis rat V beta 8.2 sequence include CDR2 and framework 3 idiotopes.
J Neurosci Res. 1996 Jan 15;43(2):137-45. doi: 10.1002/(SICI)1097-4547(19960115)43:2<137::AID-JNR2>3.0.CO;2-H.
2
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Increased severity of experimental autoimmune encephalomyelitis in rats tolerized as adults but not neonatally to a protective TCR V beta 8 CDR2 idiotope.成年而非新生期耐受保护性TCR Vβ8 CDR2独特型决定簇的大鼠实验性自身免疫性脑脊髓炎严重程度增加。
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TCR peptide therapy in human autoimmune diseases.人类自身免疫性疾病中的TCR肽疗法。
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Treatments targeting the T cell receptor (TCR): effects of TCR peptide-specific T cells on activation, migration, and encephalitogenicity of myelin basic protein-specific T cells.
靶向T细胞受体(TCR)的治疗方法:TCR肽特异性T细胞对髓鞘碱性蛋白特异性T细胞的激活、迁移及致脑炎性的影响。
Springer Semin Immunopathol. 1999;21(1):77-90. doi: 10.1007/BF00815179.
4
Regulatory T cells specific for the same framework 3 region of the Vbeta8.2 chain are involved in the control of collagen II-induced arthritis and experimental autoimmune encephalomyelitis.对Vbeta8.2链相同构架3区具有特异性的调节性T细胞参与了胶原II诱导的关节炎和实验性自身免疫性脑脊髓炎的调控。
J Exp Med. 1997 May 19;185(10):1725-33. doi: 10.1084/jem.185.10.1725.