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B Cells Influence Encephalitogenic T Cell Frequency to Myelin Oligodendrocyte Glycoprotein (MOG)38-49 during Full-length MOG Protein-Induced Demyelinating Disease.
Immunohorizons
September 2024
Division of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT.
Although T cells are encephalitogenic during demyelinating disease, B cell-depleting therapies are a successful treatment for patients with multiple sclerosis. Murine models of demyelinating disease utilizing myelin epitopes, such as myelin oligodendrocyte glycoprotein (MOG)35-55, induce a robust CD4 T cell response but mitigate the contribution of pathological B cells. This limits their efficacy for investigating how B cell depletion affects T cells.
View Article and Find Full Text PDFAdjuvant Activity of Mycobacterium paratuberculosis in Enhancing the Immunogenicity of Autoantigens During Experimental Autoimmune Encephalomyelitis.
J Vis Exp
May 2023
Department of Neurology, Juntendo University; Neurodegenerative Disorders Collaborative laboratory, RIKEN Center for Brain Science.
Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) requires immunization by a MOG peptide emulsified in complete Freund's adjuvant (CFA) containing inactivated Mycobacterium tuberculosis. The antigenic components of the mycobacterium activate dendritic cells to stimulate T-cells to produce cytokines that promote the Th1 response via toll-like receptors. Therefore, the amount and species of mycobacteria present during the antigenic challenge are directly related to the development of EAE.
View Article and Find Full Text PDFCompetitive ELISA for the identification of 35-55 myelin oligodendrocyte glycoprotein immunodominant epitope conjugated with mannan.
J Pept Sci
October 2023
Department of Chemistry, University of Patras, Rion Patras, Greece.
Analogs of immunodominant myelin peptides involved in multiple sclerosis (MS: the most common autoimmune disease) have been extensively used to modify the immune response over the progression of the disease. The immunodominant 35-55 epitope of myelin oligodendrocyte glycoprotein (MOG ) is an autoantigen appearing in MS and stimulates the encephalitogenic T cells, whereas mannan polysaccharide (Saccharomyces cerevisiae) is a carrier toward the mannose receptor of dendritic cells and macrophages. The conjugate of mannan-MOG has been extensively studied for the inhibition of chronic experimental autoimmune encephalomyelitis (EAE: an animal model of MS) by inducing antigen-specific immune tolerance against the clinical symptoms of EAE in mice.
View Article and Find Full Text PDFMyelin Basic Protein Fragmentation by Engineered Human Proteasomes with Different Catalytic Phenotypes Revealed Direct Peptide Ligands of MS-Associated and Protective HLA Class I Molecules.
Int J Mol Sci
January 2023
Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
Article Synopsis
- Proteasomes in mammalian cells are found in different variants, leading to the creation of specific immune responses, particularly in relation to multiple sclerosis (MS) and autoantigens like myelin basic protein (MBP).
- Research focused on engineered human proteasomes demonstrated that immunoproteasomes primarily produce peptides that can bind to HLA class I molecules, crucial for immune recognition.
- The study identified five important MBP peptide regions linked to MS risk, with HLA-A*44 showing a strong protective binding affinity, potentially influencing the immune system's response to autoreactive T cells in MS.
Designing and Characterization of Tregitope-Based Multi-Epitope Vaccine Against Multiple Sclerosis: An Immunoinformatic Approach.
Curr Drug Saf
February 2023
Applied Biotechnology Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Background: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system(CNS). It is widely accepted that the development and progression of MS result from aberrant activation of potentially encephalitogenic reactive-T cells against CNS antigens. The pathologic roles of both CD4+ (T helper; Th) and CD8+ T cells have been demonstrated in MS lesions.
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