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MOG (35-55)

MOG(35-55); MOG35-55; MOG 35-55; Myelin Oligodendrocyte Glycoprotein(35-55); Myelin Oligodendrocyte Glycoprotein35-55; Myelin Oligodendrocyte Glycoprotein 35-55
Met-Glu-Val-Gly-Trp-Tyr-Arg-Ser-Pro-Phe-Ser-Arg-Val-Val-His-Leu -Tyr-Arg-Asn-Gly-Lys
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Interest in MOG has centered on its role in demyelinating diseases, particularly multiple sclerosis (MS).
Myelin Oligodendrocyte Glycoprotein (MOG) is a glycoprotein believed to be important in the process of myelinization of nerves in the central nervous system (CNS). It is a transmembrane protein expressed on the surface of oligodendrocyte cell and on the outermost surface of myelin sheaths.
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Myelin oligodendrocyte glycoprotein (MOG) 35-55 is a minor component of CNS myelin. Produces a relapsing-remitting neurological disease with extensive plaque-like demyelination, common to the manifestations of multiple sclerosis. Induces strong T and B cell responses and is highly encephalitogenic.

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 moderately severe 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.

Rich, C., Link, J. M., Zamora, A., Jacobsen, H., Meza‐Romero, R., Offner, H., ... & Vandenbark, A. A. (2004). Myelin oligodendrocyte glycoprotein‐35–55 peptide induces severe chronic experimental autoimmune encephalomyelitis in HLA‐DR2‐transgenic mice. European journal of immunology, 34(5), 1251-1261.

Intravenous (i.v.) administration of encephalitogenic peptide can effectively prevent experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis; however, the underlying cellular and molecular mechanisms are not fully understood. In this study, we induced i.v. tolerance to EAE by administration of MOG(35-55) peptide and determined the effect of this approach on intracellular signaling pathways of the IL-23/IL-17 system, which is essential for the pathogenesis of MS/EAE. In tolerized mice, phosphorylation of JAK/STAT-1, -4, ERK1/2 and NF-kappaBp65 were significantly reduced in splenocytes and the central nervous system. MOG i.v. treatment led to significantly lower production of IL-17, and administration of exogenous IL-17 slightly broke immune tolerance, which was associated with reduced activation of STAT4 and NF-kappaB. Suppressed phosphorylation of these pathway molecules was primarily evident in CD11b(+) and small numbers of CD4(+), CD8(+) and CD11c(+) cells. More importantly, adoptive transfer of CD11b(+) splenocytes of tolerized mice effectively delayed onset and reduced clinical severity of actively induced EAE. This study correlates MOG i.v. tolerance with modulation of Jak/STAT signaling pathways and investigates novel therapeutic avenues for the treatment of EAE/MS.

Jiang, Z., Li, H., Fitzgerald, D. C., Zhang, G. X., & Rostami, A. (2009). MOG35–55 iv suppresses experimental autoimmune encephalomyelitis partially through modulation of Th17 and JAK/STAT pathways. European journal of immunology, 39(3), 789-799.

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