Analysis of Mannan (polymannose) Conjugated with 35-55 Immunodominant Epitope of Myelin Oligodendrocyte Glycoprotein for the Treatment of Multiple Sclerosis
Multiple sclerosis (MS) is a prevalent autoimmune disease characterised by the destruction of myelin, leading to paralysis and severe health complications.The immunodominant epitope 35-55 of myelin oligodendrocyte glycoprotein (MOG 35-55 ) is a crucial autoantigen implicated in the progression of MS.Numerous studies have focused on the use of mannan polysaccharide (derived from Saccharomyces cerevisiae) conjugated with the MOG 35-55 epitope to induce antigen-specific immune tolerance against the clinical symptoms of chronic experimental autoimmune encephalomyelitis (EAE), an animal model of MS [1,2].In this context, we present a promising approach to MS immunotherapy where the MOG 35-55 peptide is conjugated to mannan via Schiff base formation between the aldehydes of oxidised mannan and the amino groups of the (LysGly) 5 bridge located at the N-terminus of the peptide [3].To confirm the integrity of the conjugation reaction and investigate any potential alterations in the peptide throughout the different stages of mannan-MOG 35-55 conjugate production, a competitive enzyme-linked immunosorbent assay (ELISA) was developed.This assay was used in combination with sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and a colorimetric assay.These mannan-MOG 35-55 conjugates are currently undergoing a Phase I clinical trial conducted by a Greek pharmaceutical company.
Authors
- Carmen Simal (ORCID: https://orcid.org/0000-0002-7096-4281)
- Areti Gkika
- Theodore Tselios (ORCID: https://orcid.org/0000-0002-1310-0591)
- Maria‐Eleni Androutsou
- Georgia Biniari (ORCID: https://orcid.org/0009-0000-5789-8884)
- Alexios J. Aletras (ORCID: https://orcid.org/0000-0002-1209-2374)
Publication Details
- Published
- 2024-09-20
- DOI
- https://doi.org/10.17952/37eps.2024.p1151
- Primary Topic
- Biopolymer Synthesis and Applications
- Type
- article
- Field-Weighted Citation Impact
- 0.00