Multiple sclerosis: Difference between revisions

'''Multiple sclerosis (MS)''' - an autoimmune disease that effects every patient differently based on the neurologic lesions found throughout the body. While some can go through their lives with relatively mild symptoms and short periods of relapse, others can become incapacitated within years or even months. Defined by Nylander and Hafler, MS is a "multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual."<ref name ="MS Nylander & Hafler">PMID:22466660</ref> Inflammation is the primary cause of damage in MS, and though the effects of the disease are well known, and various treatments exist for the disease, the exact identity of an antigen or infectious agent that causes the initiation of a myriad of symptoms is unknown.<ref name='MS:Pathogenesis and Treatment'>PMID:22379455</ref>  

Classical MS pathology has been characterized by white matter plaques 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/1'>CD8+ T cells</scene> (two ectodomains shown, [[3qzw]]), as well as a smaller amount of <scene name='Multiple_sclerosis/Cd4tcell/1'>CD4+ T cells</scene> ([[3t0e]]), <scene name='Multiple_sclerosis/Monocyte/1'>monocytes</scene> ([[2ra4]]), and rare <scene name='Multiple_sclerosis/B_cell/1'>B cells</scene> ([[4e96]]) and <scene name='Multiple_sclerosis/Plasma_cell/1'>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/1'>T cell</scene> autoreactivity (extracellular domain shown, [[1tcr]]) in the hopes to determine a single culprit including: <scene name='Multiple_sclerosis/Mbp/1'>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" />

==Interferon-β==