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The cause and exact processes underlying the pathophysiology of multiple sclerosis (MS) development and progression have eluded clinicians and scientists for almost 150 years, since Jean-Martin Charcot recognized it as a distinct disease. Based on current understanding, an inflammatory immune response, potentially elicited by a common pathogen or unidentified microbial or environmental agent, is inappropriately targeted against CNS components, possibly a myelin protein, and not properly tempered by immune regulatory circuits. Blood-derived T and B cells are critical components of the adaptive immune response that initiates the inflammatory attack, although innate immunity is also implicated, with macrophages and microglia operating as antigen presenting cells, as demyelinating effector cells, and possibly as mediators of a diffuse chronic CNS inflammatory state.
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- © 2015 American Academy of Neurology
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