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在用致脑炎肽-载体偶联物攻击之前给予载体对实验性变应性脑脊髓炎的抑制作用。

Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide-carrier conjugate.

作者信息

Rauch H C, Montgomery I N, Swanborg R H

出版信息

Eur J Immunol. 1981 Apr;11(4):335-8. doi: 10.1002/eji.1830110413.

DOI:10.1002/eji.1830110413
PMID:6166482
Abstract

Guinea pigs can be rendered unresponsive to experimental allergic encephalomyelitis (EAE) challenge by prior injections of myelin basic protein (BP) or peptides derived from BP. The synthesized tryptophan-containing peptide (TrpP, corresponding to residues 114-122) which is the primary encephalitogenic sequence in BP (for guinea pigs) had been conjugated to the non-central nervous system protein bovine serum albumin (BSA) and used for EAE challenge. It has been shown in this study that prechallenge treatment with the BSA carrier alone can significantly inhibit the induction of EAE by TrpP-BSA conjugate. That carrier treatment is immunologically specific was determined when prior treatment with cytochrome c did not protect animals from EAE challenge with TrpP conjugated to BSA. In addition, in disease induced with BP or TrpP, and while TrpP did protect guinea pigs challenged with TrpP, it did not protect those challenged with BP. This last finding raises the possibility of a second encephalitogenic sequence in BP or an important role for the carrier in the TrpP conjugate.

摘要

豚鼠可通过预先注射髓鞘碱性蛋白(BP)或源自BP的肽,使其对实验性变应性脑脊髓炎(EAE)攻击无反应。已将在BP(针对豚鼠)中作为主要致脑炎性序列的合成含色氨酸肽(TrpP,对应于第114 - 122位残基)与非中枢神经系统蛋白牛血清白蛋白(BSA)偶联,并用于EAE攻击。本研究表明,仅用BSA载体进行攻击前治疗可显著抑制TrpP - BSA偶联物诱导的EAE。当用细胞色素c预先治疗不能保护动物免受与BSA偶联的TrpP引起的EAE攻击时,确定了载体治疗具有免疫特异性。此外,在用BP或TrpP诱导的疾病中,虽然TrpP确实保护了用TrpP攻击的豚鼠,但它不能保护用BP攻击的豚鼠。这一最新发现增加了BP中存在第二个致脑炎性序列或载体在TrpP偶联物中起重要作用的可能性。

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Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide-carrier conjugate.在用致脑炎肽-载体偶联物攻击之前给予载体对实验性变应性脑脊髓炎的抑制作用。
Eur J Immunol. 1981 Apr;11(4):335-8. doi: 10.1002/eji.1830110413.
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引用本文的文献

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Epitope-specific regulation. II. A bistable, Igh-restricted regulatory mechanism central to immunologic memory.表位特异性调节。II. 一种双稳态、受免疫球蛋白重链(Igh)限制的调节机制,是免疫记忆的核心。
J Exp Med. 1982 Jun 1;155(6):1741-53. doi: 10.1084/jem.155.6.1741.