MOG (35-55)

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.

Different MOG(35-55) concentrations induce distinguishable inflammation through early regulatory response by IL-10 and TGF-beta in mice CNS despite unchanged clinical course.[Pubmed:25585346]

Cell Immunol. 2015 Feb;293(2):87-94.

Multiple sclerosis (MS) shows distinct clinical courses. Experimental autoimmune encephalomyelitis (EAE), a model to study multiple sclerosis, can be induced by different protocols, which show distinct cytokine and antibody production. The factors involved in this heterogeneity remain unclear. The relevance of MOG concentration in triggering a regulatory response in the chronic model of EAE is imprecise. The aim of this study was investigate if 100 or 300 mug of MOG(35-55) could induce different EAE profiles. Modifications in the concentration of MOG were able to change the patterns of chemokines, cytokines, percentage of cells, inflammatory infiltrate and the development of a regulatory response. However, these changes were unable to modify the intensity of response, which explains the chronic progression of the disease in both concentrations. The results presented in this study contribute to understanding the intricate mechanisms that trigger EAE and provide insights into the pathogenesis of various forms of MS.

DRalpha1-MOG-35-55 Reduces Permanent Ischemic Brain Injury.[Pubmed:27988839]

Transl Stroke Res. 2017 Jun;8(3):284-293.

Stroke induces a catastrophic immune response that involves the global activation of peripheral leukocytes, especially T cells. The human leukocyte antigen-DRalpha1 domain linked to MOG-35-55 peptide (DRalpha1-MOG-35-55) is a partial major histocompatibility complex (MHC) class II construct which can inhibit neuroantigen-specific T cells and block binding of the cytokine/chemokine macrophage migration inhibitory factor (MIF) to its CD74 receptor on monocytes and macrophages. Here, we evaluated the therapeutic effect of DRalpha1-MOG-35-55 in a mouse model of permanent distal middle cerebral artery occlusion (dMCAO). DRalpha1-MOG-35-55 was administered to WT C57BL/6 mice by subcutaneous injection starting 4 h after the onset of ischemia followed by three daily injections. We demonstrated that DRalpha1-MOG-35-55 post treatment significantly reduced brain infarct volume, improved functional outcomes, and inhibited the accumulation of CD4(+) and CD8(+) T cells and expression of pro-inflammatory cytokines in the ischemic brain 96 h after dMCAO. In addition, DRalpha1-MOG-35-55 treatment shifted microglia/macrophages in the ischemic brain to a beneficial M2 phenotype without changing their total numbers in the brain or blood. This study demonstrates for the first time the therapeutic efficacy of the DRalpha1-MOG-35-55 construct in dMCAO across MHC class II barriers in C57BL/6 mice. This MHC-independent effect obviates the need for tissue typing and will thus greatly expedite treatment with DRalpha1-MOG-35-55 in human stroke subjects. Taken together, our findings suggest that DRalpha1-MOG-35-55 treatment may reduce ischemic brain injury by regulating post-stroke immune responses in the brain and the periphery.

A novel HLA-DRalpha1-MOG-35-55 construct treats experimental stroke.[Pubmed:24122483]

Metab Brain Dis. 2014 Mar;29(1):37-45.

Chemoattraction of leukocytes into the brain after induction of middle cerebral artery occlusion (MCAO) increases the lesion size and worsens disease outcome. Our previous studies demonstrated that partial MHC class II constructs can reverse this process. However, the potential application of pMHC to human stroke is limited by the need to rapidly match recipient MHC class II with the beta1 domain of the pMHC construct. We designed a novel recombinant protein comprised of the HLA-DRalpha1 domain linked to MOG-35-55 peptide but lacking the beta1 domain found in pMHC and treated MCAO after 4 h reperfusion in humanized DR2 mice. Infarct volumes were quantified after 96 h reperfusion and immune cells from the periphery and CNS were evaluated for expression of CD74 and other cell surface, cytokine and pathway markers. This study demonstrates that four daily treatments with DRalpha1-MOG-35-55 reduced infarct size by 40 % in the cortex, striatum and hemisphere, inhibited the migration of activated CD11b+CD45high cells from the periphery to the brain and reversed splenic atrophy. Furthermore, DRalpha1-MOG-35-55 bound to CD74 on monocytes and blocked both binding and downstream signaling of macrophage migration inhibition factor (MIF) that may play a key role in infarct development. The novel DRalpha1-MOG-35-55 construct is highly therapeutic in experimental stroke and could be given to all patients at least 4 h after stroke onset without the need for tissue typing due to universal expression of DRalpha1 in humans.

DRalpha1-MOG-35-55 treatment reduces lesion volumes and improves neurological deficits after traumatic brain injury.[Pubmed:28303450]

Metab Brain Dis. 2017 Oct;32(5):1395-1402.

Traumatic brain injury (TBI) results in severe neurological impairments without effective treatments. Inflammation appears to be an important contributor to key pathogenic events such as secondary brain injury following TBI and therefore serves as a promising target for novel therapies. We have recently demonstrated the ability of a molecular construct comprised of the human leukocyte antigen (HLA)-DRalpha1 domain linked covalently to mouse (m)MOG-35-55 peptide (DRalpha1-MOG-35-55 construct) to reduce CNS inflammation and tissue injury in animal models of multiple sclerosis and ischemic stroke. The aim of the current study was to determine if DRalpha1-MOG-35-55 treatment of a fluid percussion injury (FPI) mouse model of TBI could reduce the lesion size and improve disease outcome measures. Neurodeficits, lesion size, and immune responses were determined to evaluate the therapeutic potential and mechanisms of neuroprotection induced by DRalpha1-MOG-35-55 treatment. The results demonstrated that daily injections of DRalpha1-MOG-35-55 given after FPI significantly reduced numbers of infiltrating CD74(+) and CD86(+) macrophages and increased numbers of CD206(+) microglia in the brain concomitant with smaller lesion sizes and improvement in neurodeficits. Conversely, DRalpha1-MOG-35-55 treatment of TBI increased numbers of circulating CD11b(+) monocytes and their expression of CD74 but had no detectable effect on cell numbers or marker expression in the spleen. These results demonstrate that DRalpha1-MOG-35-55 therapy can reduce CNS inflammation and significantly improve histological and clinical outcomes after TBI. Future studies will further examine the potential of DRalpha1-MOG-35-55 for treatment of TBI.

T cell and antibody responses in remitting-relapsing experimental autoimmune encephalomyelitis in (C57BL/6 x SJL) F1 mice.[Pubmed:14975581]

J Neuroimmunol. 2004 Mar;148(1-2):1-10.

To characterize T cell and antibody responses in remitting-relapsing experimental autoimmune encephalomyelitis (RR-EAE), we compared myelin oligodendrocyte glycoprotein (MOG)-induced RR-EAE in C57BL/6 (B6) x SJL (F1) mice and chronic-progressive EAE (CP-EAE) in B6 mice at week 8 p.i. when clinical scores were comparable. Although these two strains exhibited similar inflammation/demyelination pattern and MOG-induced T cell responses, RR-EAE mice produced significantly higher levels of anti-MOG IgG1/IgG2a antibodies. Further, lymphocytes of RR-EAE mice proliferated vigorously to the secondary epitope myelin basic protein (MBP) 1-11. These results support a potential involvement of anti-MOG antibodies and epitope spreading in T cell responses in the development of MOG-induced RR-EAE model.

Induction of a multiple sclerosis-like disease in mice with an immunodominant epitope of myelin oligodendrocyte glycoprotein.[Pubmed:9771980]

Autoimmunity. 1998;28(2):109-20.

Myelin oligodendrocyte glycoprotein (MOG) is postulated to be a target autoantigen in multiple sclerosis (MS). Here we investigated the encephalitogenicity of an immunodominant epitope of MOG, peptide 35-55, in various strains of mice. An MS-like disease was induced in NOD/Lt mice (H-2g7) and C57BL/6 mice (H-2b) by a single injection of MOG35-55 in CFA. The disease followed a relapsing-remitting course in NOD/Lt mice, whereas C57BL/6 mice developed a chronic paralytic disease. Histologically, the disease in both strains was characterized by cellular infiltration and multifocal demyelination in the CNS. Significant DTH type reactions to MOG35-55 were only seen in MOG-susceptible animals, with the NOD/Lt mice showing the strongest responses. Susceptible mice also showed specific antibody responses to MOG35-55 but not to a panel of other MOG peptides. These results provide further evidence for the role of MOG as a highly autoantigenic molecule capable of inducing severe demyelinating disease.

Analysis of the fine B cell specificity during the chronic/relapsing course of a multiple sclerosis-like disease in Lewis rats injected with the encephalitogenic myelin oligodendrocyte glycoprotein peptide 35-55.[Pubmed:8752946]

J Immunol. 1996 Jul 15;157(2):919-26.

We have recently shown that a single injection of myelin oligodendrocyte glycoprotein (MOG), or the MOG35-55 peptide, produces a relapsing-remitting neurologic disease with extensive plaque-like demyelination. Given the features that this new autoimmune demyelinating model has in common with the clinicopathologic manifestations of multiple sclerosis, we have examined the Ab reactivity to native MOG and MOG35-55 peptide during the course of the disease in Lewis rats. Following immunization with MOG35-55, varied clinical symptoms were observed; these included hind and foreleg paralysis and various degrees of balance impairment. Disease progression also varied: 3 out of 21 animals had a single mild disease episode; 4 out of 21 had a mild relapsing-remitting disease; and 14 out of 21 had severe relapsing-remitting disease. Ab reactivity to MOG35-55 and native MOG was first detected in all rats 4 wk postimmunization and persisted throughout the 12 wk of observation. The Ab response was highly restricted with no reactivity to other peptides encompassing different extracellular segments of MOG. Fine epitope mapping showed that Ab from serum and cerebrospinal fluid of injected rats reacted strongly to MOG37-46 and to a lesser extent to MOG43-50. Although significant levels of anti-MOG Abs appeared necessary for the development of demyelinating lesions, their presence in blood and cerebrospinal fluid alone was not sufficient to produce severe clinical symptoms. These results demonstrate that the MOG35-55 peptide is highly encephalitogenic and can induce strong T and B cell responses. It is probably the complex interaction between these T and B cells that determines the severity of disease in individual rats.

Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat is a minor component of CNS myelin. Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat produces a relapsing-remitting neurological disease with extensive plaque-like demyelination. Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat induces strong T and B cell responses and is highly encephalitogenic.

MOG (35-55),149635-73-4,Natural Products,Neuronal Metabolism, buy MOG (35-55) , MOG (35-55) supplier , purchase MOG (35-55) , MOG (35-55) cost , MOG (35-55) manufacturer , order MOG (35-55) , high purity MOG (35-55)