Journal of Glycobiology
Open Access
ISSN: 2168-958X
ISSN: 2168-958X
Peter Koulen
Posters-Accepted Abstracts: J Glycobiol
Multiple sclerosis affecting the optic nerve and related neuroinflammatory disorders such as autoimmune optic neuritis
are characterized morphologically by significant immune cell infiltration and structural changes in nerve cells and
myelinating oligodendrocytes in parallel to impaired visual performance. When functional deficits become permanent this is
typically accompanied by damage to nerve cells such as the loss of axons in the optic nerve. Oligodendrocytes express myelin
oligodendrocyte glycoprotein (MOG), a transmembrane protein of the immunoglobulin superfamily involved in intercellular
communication at the myelin sheaths formed by oligodendrocyte around optic nerve axons. As MOG is expressed in several
isoforms, the functional importance of the extracellular domain located at the very N-terminus shared by all splice variants and
containing the site for N-linked glycosylation of the protein has become evident. Soluble peptides and recombinant proteins
derived from the MOG N-terminus were used to induce autoimmune optic neuritis. Depending on sequence, length, dosing
and timing of administration delivery of the MOG peptides and proteins differential effects were observed in disease models
using functional markers of neuroinflammation such as demyelination and immune cell infiltration. Specifically, expression
levels and distribution of proteins typically found in highly localized expression patterns within axons were significantly altered
depending on the MOG-derived peptide constructs. This was paralleled by functional impairment at the cellular and organ
level. Altogether, peptides and recombinant proteins derived from the MOG N-terminus can be used selectively in research
models to recapitulate differential patterns and aspects of structural and functional damage of autoimmune optic neuritis.