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

被引:17
作者
Badawi, Ahmed H. [1 ]
Siahaan, Teruna J. [1 ]
机构
[1] Univ Kansas, Dept Pharmaceut Chem, Lawrence, KS 66047 USA
基金
美国国家卫生研究院;
关键词
Experimental autoimmune encephalomyelitis; Bifunctional peptide inhibitor; Antigen-presenting cell; T cell; Epitope spreading; CENTRAL-NERVOUS-SYSTEM; MYELIN BASIC-PROTEIN; ANTIGEN-SPECIFIC SUPPRESSION; IMMUNOLOGICAL SYNAPSE; PROTEOLIPID PROTEIN; GLATIRAMER ACETATE; SELF-RECOGNITION; T-CELLS; BLOOD; REGRESSION;
D O I
10.1016/j.jneuroim.2013.07.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
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 (MOG(38-50)) and myelin proteolipid protein (PLP138-151) was evaluated in suppressing MOG(38-50)(-) and PLP139-151-induced EAE. MVBMOG/PLP significantly suppressed both models of EAE even when there was some evidence of epitope spreading in the MOG(38-50)-induced EAE model. In addition, MVBMOG/PLP was found to be more effective than PLP-BPI and MOG-BPI in suppressing MOG(38-50)-induced EAE. Thus, the development of MVB molecules with broader antigenic targets can lead to suppression of epitope spreading in EAE. (C) 2013 Elsevier B.V. All rights reserved.
引用
收藏
页码:20 / 27
页数:8
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