Multiple sclerosis: Difference between revisions
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== Immunopathology== | == Immunopathology== | ||
Classical MS pathology has been characterized by white matter plaques, shown in the picture above, which are typically located in the subcortical or periventricular white matter, optic nerve sheaths, brain stem, and spinal cord. The lesions that occur in these regions are generally identified by perivascular infiltrates that contain clonally expanded <scene name='Multiple_sclerosis/Cd8tcell/ | Classical MS pathology has been characterized by white matter plaques, shown in the picture above, which are typically located in the subcortical or periventricular white matter, optic nerve sheaths, brain stem, and spinal cord. The lesions that occur in these regions are generally identified by perivascular infiltrates that contain clonally expanded <scene name='Multiple_sclerosis/Cd8tcell/2'>CD8+ T cells</scene> (two ectodomains shown, [[3qzw]]), as well as a smaller amount of <scene name='Multiple_sclerosis/Cd4tcell/2'>CD4+ T cells</scene> ([[3t0e]]), <scene name='Multiple_sclerosis/Monocyte/2'>monocytes</scene> ([[2ra4]]), and rare <scene name='Multiple_sclerosis/B_cell/2'>B cells</scene> ([[4e96]]) and <scene name='Multiple_sclerosis/Plasma_cell/2'>plasma cells</scene> ([[2wq9]]). Pathologists disagree on whether there are different mechanisms for the inflammatory and degenerative components of MS, especially given that older patients have generally progressed further along with their degeneration. There are many proposed degeneration mechanisms including Wallerian degeneration secondary to demyelination, and axonal transection, damage from reactive oxygen species and nitric oxide, or energy failure from mitochondrial dysfunction.<ref name="MS Nylander & Hafler" /><ref>PMID:20477831</ref><ref>PMID:12849456</ref><ref>PMID:21446022</ref> Many antigens have been investigated to determine whether they are the cause of <scene name='Multiple_sclerosis/Xtracllulrtcell/2'>T cell</scene> autoreactivity (extracellular domain shown, [[1tcr]]) in the hopes to determine a single culprit including: <scene name='Multiple_sclerosis/Mbp/2'>myelin basic protein</scene> (MBP, [[1bx2]]) with a peptide shown; <scene name='Multiple_sclerosis/Plp/1'>proteolipid protein</scene> (PLP, [[2xpg]]) with peptide shown; <scene name='Multiple_sclerosis/Mog/1'>oligodendrocyte glycoprotein</scene> (MOG, [[3csp]]); oligodendroglia-specific enzyme transaldolase, and heat shock protein <scene name='Multiple_sclerosis/Alphabcrystallin/1'>alphaB crystallin</scene> ([[2y1z]]).<ref name="MS Nylander & Hafler" /> | ||
Interesting discoveries have been made on possible inhibitors of myelin repair functions within the body, with an obvious application to MS treatment. The structure of the <scene name='Multiple_sclerosis/Lingo-1ectodomain/1'>lingo-1 ectodomain</scene> is a module implicated in central nervous system repair inhibition. The interactions of lingo-1 with receptors lead to neurite and axonal collapse. Lingo- 1 also regulates oligodendrocyte differentiation and myelination, thus leading to the suggestion that pharmacological modulation of Lingo-1 function could be a novel approach for nerve repair and remyelination therapies.<ref name='Lingo-1'>PMID:17005555</ref> | Interesting discoveries have been made on possible inhibitors of myelin repair functions within the body, with an obvious application to MS treatment. The structure of the <scene name='Multiple_sclerosis/Lingo-1ectodomain/1'>lingo-1 ectodomain</scene> is a module implicated in central nervous system repair inhibition. The interactions of lingo-1 with receptors lead to neurite and axonal collapse. Lingo- 1 also regulates oligodendrocyte differentiation and myelination, thus leading to the suggestion that pharmacological modulation of Lingo-1 function could be a novel approach for nerve repair and remyelination therapies.<ref name='Lingo-1'>PMID:17005555</ref> | ||
