Format

Send to

Choose Destination
See comment in PubMed Commons below
Immunology. 2013 Dec;140(4):456-64. doi: 10.1111/imm.12155.

Novel pathogenic epitopes of myelin oligodendrocyte glycoprotein induce experimental autoimmune encephalomyelitis in C57BL/6 mice.

Author information

1
ICM - Hôpital Pitié-Salpêtrière, INSERM UMRS 975/UPMC/CNRS UMR7225, Paris, France.

Abstract

Myelin oligodendrocyte glycoprotein (MOG), a minor protein of the central nervous system myelin, is recognized as a potential target in multiple sclerosis and neuromyelitis optica. The extracellular domain of MOG is commonly used in a wide range of mouse strains and other animals to induce experimental autoimmune encephalomyelitis (EAE), an autoimmune animal model of multiple sclerosis, because it is a target for antibody-mediated attack. Previous studies, using selected peptides, have indicated that MOG(35-55) peptide is an encephalitogenic epitope in C57BL/6 (H-2(b)) mice. A more systematic analysis of both T-cell and B-cell responses following immunization of C57BL/6 mice with either recombinant extracellular mouse MOG protein (1-116) or with overlapping peptides spanning the whole sequence of MOG, before assessment of responses to 15 mer and 23 mer peptides was undertaken. The studies identified T-cell responses within the MOG(35-55) (extracellular domain) but also two new immunogenic and encephalitogenic T-cell epitopes within residues MOG(113-127), MOG(120-134) (localized in the transmembrane region) and MOG(183-197) (in the second hydrophobic MOG domain). In addition, residue MOG(113-127) was found to be a B-cell epitope, suggesting that this may be a useful adjunct for the induction of EAE as well as for immunological studies in C57BL/6 mice, which are increasingly being used to study immune function through the use of transgenic and gene knockout technology.

KEYWORDS:

C57BL/6; epitope; experimental autoimmune encephalomyelitis; mouse; multiple sclerosis; peptide

PMID:
23876060
PMCID:
PMC3839649
DOI:
10.1111/imm.12155
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Support Center