This historical experiment used transgenic mice. Human and mouse MOG peptides produced different effects; the proposed relevance to human disease required further study. It does not establish a cause of MS in people.
Eur J Immunol. 2004 May;34(5):1251-61
Rich C, Link JM, Zamora A, Jacobsen H, Meza-Romero R, Offner H, Jones R, Burrows GG, Fugger L, Vandenbark AA.
Veterans Affairs Medical Center, Portland, USA.
The use of HLA class II-transgenic (Tg) mice has facilitated identification of antigenic T cell epitopes that may contribute to inflammation in T cell-mediated diseases such as rheumatoid arthritis and multiple sclerosis (MS).
In this study, we compared the encephalitogenic activity of three DR2-restricted myelin determinants [mouse (m) myelin oligodendrocyte glycoprotein (MOG)-35-55, human (h)MOG-35-55 and myelin basic protein (MBP)-87-99] in Tg mice expressing the MS-associated DR2 allele, DRB1*1501.
We found that mMOG-35-55 peptide was strongly immunogenic and induced moderatelysevere chronic experimental autoimmune encephalomyelitis (EAE) with white matter lesions after a single injection in Freund's complete adjuvant followed by pertussis toxin.
hMOG-35-55 peptide,which differs from mMOG-35-55 peptide by a proline for serine substitution at position 42, was also immunogenic, but not encephalitogenic, and was only partially cross-reactive with mMOG-35-55.
In contrast, MBP-87-99, which can induce EAE in double-Tg mice expressing both HLA-DR2 and a human MBP-specific TCR, was completely non-encephalitogenic in HLA-DR2-Tg mice lacking the human TCR transgene.
These findings demonstrate potent encephalitogenic activity of the mMOG-35-55 peptide in association with HLA-DR2, thus providing a strong rationale for further study of hMOG-35-55 peptide as a potential pathogenic determinant in humans.
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Author: Rich C, Link JM, Zamora A, Jacobsen H, Meza-Romero R, Offner H, Jones R, Burrows GG, Fugger L, Vandenbark AA.
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