共 36 条
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.
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页码:20 / 27
页数:8
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