title: Immunologic mechanisms of multiple sclerosis.
abstract: Multiple sclerosis is widely recognized as the most commonly identified cause of progressive neurologic disability in young adults throughout the developed world. The disorder is clinically suspected when patients experience either acute attacks of neurologic compromise or instead are afflicted by a steadily progressive deterioration in functional capabilities. The pathophysiology of acute exacerbations is thought to be related to the development of inflammation and its consequences, within strategic and often discrete central nervous system tract systems. Although a myriad of hypotheses have been formulated to explain the underpinnings of the mechanisms that contribute to both the predilection and triggering of the multiphasic inflammatory events that personify multiple sclerosis, much remains to be done to understand fully the specific set and sequence of events that produce the disease and its cardinal features.
authors.affiliation: Department of Neurology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75235, USA. elliot.frohman@utsouthwestern.edu
authors.forename: Elliot M
authors.initials: EM
authors.lastname: Frohman
authors.forename: Todd
authors.initials: T
authors.lastname: Eagar
authors.forename: Nancy
authors.initials: N
authors.lastname: Monson
authors.forename: Olaf
authors.initials: O
authors.lastname: Stuve
authors.forename: Nitin
authors.initials: N
authors.lastname: Karandikar
mesh_terms: D006801:Humans; D007249:Inflammation / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D008214:Lymphocytes / Q000502:physiology; D009103:Multiple Sclerosis / Q000276:immunology* / Q000473:pathology* / Q000503:physiopathology; D009416:Nerve Regeneration / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology