Suppression of MOG- and PLP-induced experimental autoimmune encephalomyelitis using a novel multivalent bifunctional peptide inhibitor.
Suppression of MOG- and PLP-induced experimental autoimmune encephalomyelitis using a novel multivalent bifunctional peptide inhibitor.
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DOI：
10.1016/j.jneuroim.2013.07.009
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发表时间：
2013-10-15
影响因子：
3.3
通讯作者：
Siahaan, Teruna J.
中科院分区：
文献类型：
--
作者：
Badawi, Ahmed H.;Siahaan, Teruna J.
关键词：
以前，双功能多肽抑制剂(BPI)与单一抗原肽一起被证明以抗原特异性的方式抑制实验性自身免疫性脑脊髓炎(EAE)。本研究评价了含有髓鞘少突胶质细胞糖蛋白(MOG38-50)和髓鞘蛋白脂蛋白(PLP139-151)两种抗原肽的多价BPI(MVBMOG/PLP)对MOG38-50和PLP139-151诱导的EAE的抑制作用。即使在MOG38-50诱导的EAE模型中有一些表位扩散的证据，MVBMOG/PLP也显著抑制了这两种EAE模型。此外，MVBMOG/PLP在抑制MOG38-50诱导的EAE方面比PLP-BPI和MOG-BPI更有效。因此，开发具有更广泛抗原靶点的MVB分子可以抑制EAE中的表位扩散。
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.
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