Myelin oligodendrocyte glycoprotein (MOG) is a type I integral membrane protein on the extracellular surface of oligodendrocytes in the outermost lamellae of the myelin sheath. MOG can exist as monomeric and dimeric species. Its extracellular localisation facilitates its functions as a homophilic adhesion receptor, where it plays a role in the completion, compaction and maintenance of the myelin.
Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disorder of the central nervous system (CNS) characterized by myelin destruction and axonal degeneration. MOG has been identified as a key autoantigen for demyelination in MS and experimental autoimmune encephalomyelitis (EAE), an animal model that resembles MS. Although MOG is a minor component of the CNS, it is highly immunogenic and can stimulate the activation of T-cell and B-cell responses.
Immunization of rodents with native or recombinant MOG or synthetic MOG derived peptides induces an inflammatory response and initiates an immune response against myelin, causing damage and degeneration of the CNS. A number of MOG peptide fragments have shown to be encephalitogenic determinants, including MOG (1-22), MOG (35-55), MOG (92-106). Crystal structure studies of the MOG extracellular domain in a homodimer complex reveal that residues within the MOG 1-22, 35-55 and 92-106 map onto the face of the β-sheet and participate in the dimerization interface. This suggests a link between the dimeric form of MOG and a failure of immunological tolerance to MOG seen in MS.
Studies using various MOG derived peptides show that the MOG (35-55) fragment is the most potent encephalitogen and the immunodominant epitope for T cell response. MOG (35-55) induced EAE models can be used to recapitulate all three MS subtypes, which are relapsing-remitting MS (RRMS), primary progressive MS (PPMS) and secondary progressive MS (SPMS). Depending on the MOG (35-55) dose, immunized mice are presented with varying degrees of neuropathogical impairment, immune infiltration, ascending paralysis, demyelinating lesions, axon loss and gliosis in the spinal cord and brain. MOG (35-55) induced EAE models can provide an insight into elucidating the immunopathological mechanism of MS progression and facilitate in the development of novel therapeutics.
MOG (35-55) acid Mouse, Rat
MOG (35-55) amide Mouse, Rat
MOG (92-106) Mouse, Rat