Suppression of MOG- and PLP-Induced Experimental Autoimmune Encephalomyelitis Using a Novel Multivalent Bifunctional Peptide Inhibitor
dc.contributor.author | Badawi, Ahmed H. | |
dc.contributor.author | Siahaan, Teruna J. | |
dc.date.accessioned | 2017-05-24T17:50:29Z | |
dc.date.available | 2017-05-24T17:50:29Z | |
dc.date.issued | 2013-10-15 | |
dc.identifier.citation | Badawi, A. H., & Siahaan, T. J. (2013). Suppression of MOG- and PLP-Induced Experimental Autoimmune Encephalomyelitis Using a Novel Multivalent Bifunctional Peptide Inhibitor. Journal of Neuroimmunology, 263(0), 20–27. http://doi.org/10.1016/j.jneuroim.2013.07.009 | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/24299 | |
dc.description.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. | en_US |
dc.publisher | Elsevier | en_US |
dc.rights | This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | en_US |
dc.subject | Experimental autoimmune encephalomyelitis | en_US |
dc.subject | Bifunctional peptide inhibitor | en_US |
dc.subject | Antigen-presenting cell | en_US |
dc.subject | T cell | en_US |
dc.subject | Epitope spreading | en_US |
dc.title | Suppression of MOG- and PLP-Induced Experimental Autoimmune Encephalomyelitis Using a Novel Multivalent Bifunctional Peptide Inhibitor | en_US |
dc.type | Article | en_US |
kusw.kuauthor | Badawi, Ahmed H. | |
kusw.kuauthor | Siahaan, Teruna J. | |
kusw.kudepartment | Pharmaceutical Chemistry | en_US |
kusw.oanotes | Per SHERPA/RoMEO 5/24/2017: Author's Pre-print: green tick author can archive pre-print (ie pre-refereeing) Author's Post-print: green tick author can archive post-print (ie final draft post-refereeing) Publisher's Version/PDF: cross author cannot archive publisher's version/PDF General Conditions: Authors pre-print on any website, including arXiv and RePEC Author's post-print on author's personal website immediately Author's post-print on open access repository after an embargo period of between 12 months and 48 months Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months Author's post-print may be used to update arXiv and RepEC Publisher's version/PDF cannot be used Must link to publisher version with DOI Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License | en_US |
dc.identifier.doi | 10.1016/j.jneuroim.2013.07.009 | en_US |
kusw.oaversion | Scholarly/refereed, author accepted manuscript | en_US |
kusw.oapolicy | This item meets KU Open Access policy criteria. | en_US |
dc.identifier.pmid | PMC4139121 | en_US |
dc.rights.accessrights | openAccess |
Files in this item
This item appears in the following Collection(s)
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.