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.
CAT No: 10-101-57
CAS No:163913-87-9
Synonyms/Alias:PMG-3660-PI;MOG (Rat, Mouse, 35-55);163913-87-9;H-Met-Glu-Val-Gly-Trp-Tyr-Arg-Ser-Pro-Phe-Ser-Arg-Val-Val-His-Leu-Tyr-Ar g-Asn-Gly-Lys-OH; Myelin Oligodendrocyte Protein (35-55); MOG (35-55); MEVGWYRSPFSRVVHLYRNGK;
MOG (35-55) is a synthetic peptide fragment corresponding to residues 35 to 55 of the myelin oligodendrocyte glycoprotein, a key component of the central nervous system myelin sheath. As a well-characterized immunodominant epitope, this peptide is widely utilized in neuroimmunological research, particularly in studies modeling demyelinating diseases such as multiple sclerosis. Its sequence is highly conserved among rodents, making it especially relevant for experimental autoimmune encephalomyelitis (EAE) models. The ability of this peptide to induce robust and reproducible immune responses has positioned it as an essential tool for elucidating mechanisms of neuroinflammation, myelin damage, and T cell-mediated autoimmunity.
Autoimmune Disease Modeling: MOG (35-55) is extensively employed in the induction of experimental autoimmune encephalomyelitis in susceptible mouse and rat strains. By triggering a targeted immune response against myelin, the peptide enables researchers to simulate key pathological features of multiple sclerosis, including demyelination, axonal loss, and infiltration of immune cells into the central nervous system. Such in vivo models are indispensable for dissecting the cellular and molecular events underlying autoimmune neurodegeneration and for evaluating the efficacy of novel immunomodulatory strategies.
Immunological Mechanism Studies: The peptide serves as a defined antigen for probing T cell recognition and activation in the context of central nervous system autoimmunity. Using MOG (35-55), investigators can isolate, characterize, and track antigen-specific CD4+ T lymphocytes, enabling detailed analysis of T cell receptor specificity, cytokine production profiles, and cellular differentiation pathways. These studies contribute to a deeper understanding of the immunopathological processes that drive inflammatory demyelination and inform the development of targeted interventions.
Antigen Presentation Research: MOG (35-55) provides a reliable substrate for examining the mechanisms of antigen processing and presentation by major histocompatibility complex class II molecules. Its defined sequence and strong immunogenicity facilitate in vitro assays with antigen-presenting cells, allowing for the study of peptide-MHC binding, presentation efficiency, and modulation by co-stimulatory signals. Insights gained from such experiments are critical for unraveling the interplay between innate and adaptive immunity in neuroinflammatory contexts.
Vaccine and Tolerance Protocol Development: The peptide is an important reagent in the design and optimization of antigen-specific tolerance induction protocols. By leveraging its well-characterized immunogenic properties, researchers can evaluate various immunization regimens, adjuvant formulations, and delivery systems aimed at modulating immune responses to myelin antigens. These investigations are pivotal for the preclinical assessment of strategies intended to prevent or attenuate autoimmunity without broadly suppressing immune function.
In vitro Assays and Cellular Functional Studies: MOG (35-55) is widely used in ex vivo and in vitro experimental setups to stimulate lymphocytes from immunized animals or patient-derived samples. Its application enables the measurement of proliferation, cytokine secretion, and cytotoxic activity of antigen-specific T cells. Such functional assays are critical for validating immune responses, screening pharmacological inhibitors, and characterizing the role of individual immune cell subsets in the context of myelin antigen recognition and neuroinflammation.
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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