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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Suppression of MOG- and PLP-induced experimental autoimmune encephalomyelitis using a novel multivalent bifunctional peptide inhibitor
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Suppression of MOG- and PLP-induced experimental autoimmune encephalomyelitis using a novel multivalent bifunctional peptide inhibitor

机译: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

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摘要

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.
机译:以前,具有单一抗原肽的双功能肽抑制剂(BPI)已显示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,评估了多价BPI(MVBMOG / PLP)和两种衍生自髓磷脂少突胶质细胞糖蛋白(MOG38-50)和髓磷脂蛋白脂蛋白(PLP139-151)的抗原肽在抑制MOG38-50和PLP139-151诱导的EAE中的作用。 MVBMOG / PLP显着抑制了两种EAE模型,即使在MOG38-50诱导的EAE模型中存在一些表位扩散的证据时也是如此。另外,发现MVBMOG / PLP在抑制MOG38-50诱导的EAE方面比PLP-BPI和MOG-BPI更有效。因此,具有更广泛的抗原靶标的MVB分子的发展可以导致抑制在EAE中扩展的表位。

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