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本文引用的文献

1
Controlling immune response and demyelination using highly potent bifunctional peptide inhibitors in the suppression of experimental autoimmune encephalomyelitis.使用高效双功能肽抑制剂控制免疫反应和脱髓鞘，以抑制实验性自身免疫性脑脊髓炎。
Clin Exp Immunol. 2013 Apr;172(1):23-36. doi: 10.1111/cei.12029.
2
Suppression of EAE and prevention of blood-brain barrier breakdown after vaccination with novel bifunctional peptide inhibitor.新型双功能肽抑制剂疫苗接种抑制 EAE 和预防血脑屏障破坏。
Neuropharmacology. 2012 Mar;62(4):1874-81. doi: 10.1016/j.neuropharm.2011.12.013. Epub 2011 Dec 17.
3
Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases.利用 BPI 和当前的自身免疫性疾病疗法特异性阻断 CD4 特异性免疫突触的形成。
Med Res Rev. 2012 Jul;32(4):727-64. doi: 10.1002/med.20243. Epub 2011 Mar 23.
4
Immune cell entry to central nervous system--current understanding and prospective therapeutic targets.免疫细胞进入中枢神经系统——当前的认识及潜在治疗靶点。
Endocr Metab Immune Disord Drug Targets. 2009 Dec;9(4):315-27. doi: 10.2174/187153009789839219.
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Antigen-specific suppression of experimental autoimmune encephalomyelitis by a novel bifunctional peptide inhibitor: structure optimization and pharmacokinetics.新型双功能肽抑制剂对实验性自身免疫性脑脊髓炎的抗原特异性抑制作用：结构优化和药代动力学。
J Pharmacol Exp Ther. 2010 Mar;332(3):1136-45. doi: 10.1124/jpet.109.161109. Epub 2009 Dec 21.
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Preferential recruitment of interferon-gamma-expressing TH17 cells in multiple sclerosis.多发性硬化症中表达干扰素-γ的TH17细胞的优先募集。
Ann Neurol. 2009 Sep;66(3):390-402. doi: 10.1002/ana.21748.
7
Immune response to controlled release of immunomodulating peptides in a murine experimental autoimmune encephalomyelitis (EAE) model.免疫调节肽控释在实验性自身免疫性脑脊髓炎（EAE）模型中的免疫反应。
J Control Release. 2010 Jan 25;141(2):145-52. doi: 10.1016/j.jconrel.2009.09.002. Epub 2009 Sep 12.
8
Prophylactic and therapeutic suppression of experimental autoimmune encephalomyelitis by a novel bifunctional peptide inhibitor.一种新型双功能肽抑制剂对实验性自身免疫性脑脊髓炎的预防性和治疗性抑制作用
Clin Immunol. 2008 Oct;129(1):69-79. doi: 10.1016/j.clim.2008.06.002. Epub 2008 Aug 3.
9
IL-6 blockade inhibits the induction of myelin antigen-specific Th17 cells and Th1 cells in experimental autoimmune encephalomyelitis.白细胞介素-6阻断可抑制实验性自身免疫性脑脊髓炎中髓鞘抗原特异性Th17细胞和Th1细胞的诱导。
Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9041-6. doi: 10.1073/pnas.0802218105. Epub 2008 Jun 24.
10
Suppression of type 1 diabetes in NOD mice by bifunctional peptide inhibitor: modulation of the immunological synapse formation.双功能肽抑制剂对非肥胖糖尿病（NOD）小鼠1型糖尿病的抑制作用：免疫突触形成的调节
Chem Biol Drug Des. 2007 Sep;70(3):227-36. doi: 10.1111/j.1747-0285.2007.00552.x.

使用新型多价双功能肽抑制剂抑制 MOG 和 PLP 诱导的实验性自身免疫性脑脊髓炎。

Suppression of MOG- and PLP-induced experimental autoimmune encephalomyelitis using a novel multivalent bifunctional peptide inhibitor.

机构信息

Department of Pharmaceutical Chemistry, University of Kansas, Lawrence, KS 66047, United States.

出版信息

J Neuroimmunol. 2013 Oct 15;263(1-2):20-7. doi: 10.1016/j.jneuroim.2013.07.009. Epub 2013 Aug 1.

DOI:10.1016/j.jneuroim.2013.07.009
PMID:23911075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4139121/
Abstract

Previously, bifunctional peptide inhibitors (BPI) with a single antigenic peptide have been shown to suppress experimental autoimmune encephalomyelitis (EAE) in an antigen-specific manner. In this study, a multivalent BPI (MVBMOG/PLP) with two antigenic peptides derived from myelin oligodendrocyte glycoprotein (MOG38-50) and myelin proteolipid protein (PLP139-151) was evaluated in suppressing MOG38-50- and PLP139-151-induced EAE. MVBMOG/PLP significantly suppressed both models of EAE even when there was some evidence of epitope spreading in the MOG38-50-induced EAE model. In addition, MVBMOG/PLP was found to be more effective than PLP-BPI and MOG-BPI in suppressing MOG38-50-induced EAE. Thus, the development of MVB molecules with broader antigenic targets can lead to suppression of epitope spreading in EAE.

摘要

先前，具有单一抗原肽的双功能肽抑制剂 (BPI) 已被证明能够以抗原特异性方式抑制实验性自身免疫性脑脊髓炎 (EAE)。在这项研究中，评估了一种具有两个抗原肽的多价 BPI (MVBMOG/PLP)，这两个抗原肽来源于髓鞘少突胶质细胞糖蛋白 (MOG38-50) 和髓鞘蛋白脂质蛋白 (PLP139-151)，以抑制 MOG38-50- 和 PLP139-151 诱导的 EAE。即使在 MOG38-50 诱导的 EAE 模型中出现表位扩展的一些证据时，MVBMOG/PLP 也显著抑制了这两种 EAE 模型。此外，与 PLP-BPI 和 MOG-BPI 相比，MVBMOG/PLP 更有效地抑制了 MOG38-50 诱导的 EAE。因此，开发具有更广泛抗原靶标的 MVB 分子可以导致 EAE 中表位扩展的抑制。