Myelin Basic Protein (MBP) is a myelin sheath protein ordinarily sequestered fro
ID: 74467 • Letter: M
Question
Myelin Basic Protein (MBP) is a myelin sheath protein ordinarily sequestered from the immune system. Injecting myelin basic protein (MBP) with adjuvant into a mouse induces an autoimmune condition reminiscent of Multiple Sclerosis (MS) called experimental autoimmune encephalomyelitis (EAE). EAE has been used as a model for testing potential drugs to treat multiple sclerosis. In EAE, the mouse's immune system attacks MBP in myelin sheaths, but also attacks other sequestered proteins in the myelin sheath (for example, Myelin Proteolipid Protein and Myelin Oligodendrocyte Glycoprotein) even though the mouse was not immunized with them. Why are these other antigens attacked?Explanation / Answer
SOLUTION:
Multiple sclerosis is an autoimmune disease of the central nervous system characterized by primary demyelination, is result from an autoimmune attack against myelin components.
Experimental autoimmune encephalomyelitis (EAE), in the mouse immune system attack (MBP) in myelin sheath.
For MS, the quantitatively major malign proteins are myelin basic protein (MBP) and proteolipid protein (PLP) have been extensively studied as the relevant primary antigens in MS, and therapeutic approaches have been targeted to counteract autoimmune reactivity to MBP and PLP.
Reason of other antigen attacked because copolymer 1, a random synthetic amino acid copolymer cross-reactive with MBP and highly protective against the induction of EAE with MBP or PLP, is not being extensively tested in clinical studies as a therapeutic agent for MS.
These increasing reasons suggest that autoimmune reactivity against other CNS-specific myelin proteins could also be involved in the pathogenesis of MS.
Induction of a differentially expressed disease in different strains of mice with the same myelin antigen makes this new model particularly relevant to MS, where different expression of the disease is seen in different patients.
The importance of the autoimmune reactivity to MBP and PLP in MS, the potentially pathogenic autoimmune reactivity to MOG
The possible effect of copolymer 1 treatment of autoimmune reactivity to MOG(myelin oligodendrocyte glycoprotein) and on the development of EAE induced by MOG.
Copolymer 1 was found to inhibit the binding of MOG peptides to MHC molecules.
MOG peptide exerted a strong protective effect against the development of EAE.
Effect of copolymer 1 on the autoimmune response to MOG in mice indicate that copolymer 1 may also be effective in cases of MS.
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