Multiple sclerosis is an autoimmune disease.
The cause is unknown, but it appears to involve a combination of genetic susceptibility and a nongenetic trigger, such as a virus, metabolism, or environmental factors, that together result in a self-sustaining autoimmune disorder that leads to recurrent immune attacks on the CNS.
It is proposed that an unknown non-self antigen mimics proteins in myelin. This antigen is presented on the surface of macrophages in combination with class 2 MHC.
The resulting stimulation of Th1 T helper lymphocytes causes their expression of LFA-1 and VLA-4. These T helper cells may now bind to the cognate adhesion molecules, ICAM-1 and VCAM-1, on vascular endothelial cells. The release of proteases permits the T helper cells to cross the endothelium and enter the central nervous system.
The destruction of myelin proceeds in three ways:
Multiple sclerosis has classically been considered to be primarily a demyelinating disease. It is clear that neuronal death occurs from the early stages of the disease. It is probably this process of neuronal loss which contributes to the accumulating disability in multiple sclerosis.
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