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

• A novel peptide composed of MOG and an adhesion peptide was tested in EAE.
• Another peptide composed of 2 myelin antigens and an adhesion peptide was tested.
• MOG-BPI suppressed disease significantly when tested in MOG-induced EAE.
• MVPMOG/PLP was able to suppress both MOG- and PLP-induced EAE.

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.