For this aim, mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55), followed by pertussis toxin to induce paralysis in EAE mice.
In autoantibody-associated demyelinating syndromes such as neuromyelitis optica (NMO) and in myelin-oligodendrocyte-glycoprotein-(MOG)-autoantibody-associated encephalomyelitis, B-cells are a logical target based on the pathogenesis of these antibody-mediated disorders.
In order to establish whether such T cell responses are likely to be antigen-specific particularly with regard to myelin basic protein (MBP), we analysed T-cell receptor (TCR) gene rearrangements directly from MS brain plaques, using the polymerase chain reaction on reverse transcribed messenger RNA, and compared these with TCR of previously described MBP-specific T cell clones from MS and the rat model experimental allergic encephalomyelitis.
Several regions identified in myelin basic protein and P2 protein can be related to experimental allergic encephalomyelitis or neuritis in laboratory animals.
We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS, mice with experimental autoimmune encephalomyelitis (EAE), which was induced by myelin oligodendrocyte glycoprotein 35-55 peptides.
We also show that DNA vaccines can be used to reverse established EAE by covaccination with the genes for myelin oligodendrocyte glycoprotein and IL-4.
Induction of EAE caused a significant decrease of myelin basic protein expression in the hindbrain of disease affected WT mice in comparison to Cpt1a P479L mice.
In this study, the expression of IL-17, hypoxia inducible factor-1α (HIF-1α), IL-1β, IL-6 and microRNA-497 (miR-497), as well as their intrinsic associations, was investigated using EAE model mice and cultured astrocytes exposed to IL-17 in vitro.
Antibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with a unique acquired central nervous system demyelinating disease-termed MOG-IgG-associated disorder (MOGAD)-which has a variety of clinical manifestations, including optic neuritis, transverse myelitis, acute disseminating encephalomyelitis, and brainstem encephalitis.
Treatment with a DNA vaccine encoding myelin basic protein peptide 68-85 and containing three ISS of 5'-AACGTT-3' sequence suppressed clinical signs of EAE, while a corresponding DNA vaccine without such ISS had no effect.
Mice were immunized with murine myelin oligodendrocyte glycoprotein (MOG) peptides and at the onset of EAE symptoms, were treated every other day with either WE thrombin (25 μg/kg; i.v.), a selective recombinant protein C activator thrombin analog, or saline control.
In contrast, in MOG p35-55-induced EAE, B cells did not become activated or efficiently polarize proinflammatory MOG-specific T cells, similar to naive B cells.
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.
Immunization with PLP(91-110) peptide caused atypical EAE in DRB1*0301.DQ8.IFN-γ(-/-) mice characterized by ataxia, spasticity, and dystonia, hallmarks of brain-specific disease.
Carnosol treatment significantly alleviated clinical development in the myelin oligodendrocyte glycoprotein (MOG<sub>35-55</sub>) peptide-induced EAE model, markedly decreased inflammatory cell infiltration into the central nervous system and reduced demyelination.
The role of the humoral phase of the immune response in development of T cell-mediated experimental allergic encephalomyelitis (EAE) had not been clearly defined previously even though studies of the myelin basic protein (MBP) molecule had demonstrated the presence not only of T cell but also B cell epitopes capable of inducing cell-mediated immunity and antibody formation.
The rats in the EAE group were injected intraperitoneally with myelin oligodendrocyte glycoprotein 35-55 emulsion, and those in the control group were injected with the equivalent volume of normal saline.
Major histocompatibility complex (MHC) class II and T-cell receptor (TCR) gene polymorphisms play important roles in rodent susceptibility to EAE and were analyzed to determine if the same was true in humans with SAE.
Correction to: Nebulization of RNS60, a Physically-Modified Saline, Attenuates the Adoptive Transfer of Experimental Allergic Encephalomyelitis in Mice: Implications for Multiple Sclerosis Therapy.