B cells and antibodies in CNS demyelinating disease.
There is much evidence to implicate B cells, plasma cells, and their products in the pathogenesis of MS. Despite unequivocal evidence that the animal model for MS, EAE, is initiated by myelin-specific T cells, there is accumulating evidence of a role for B cells, plasma cells, and their products in EAE pathogenesis. The role(s) played by B cells, plasma cells, and antibodies in CNS inflammatory demyelinating diseases are likely to be multifactorial and complex, involving distinct and perhaps opposing roles for B cells versus antibody.
Cross
A H
AH
Department of Neurology and Neurosurgery, Washington University School of Medicine, Box 8111, 660 S. Euclid, St. Louis, MO 63110, USA. crossa@neuro.wustl.edu
Trotter
J L
JL
Lyons
J
J
D000818:Animals; D000906:Antibodies / Q000502:physiology*; D017951:Antigen Presentation; D000936:Antigen-Antibody Complex / Q000502:physiology; D001323:Autoantibodies / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000502:physiology*; D001921:Brain / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology* / Q000276:immunology; D006801:Humans; D009103:Multiple Sclerosis / Q000209:etiology* / Q000276:immunology; D010587:Phagocytosis; D010950:Plasma Cells / Q000502:physiology
D000906:Antibodies; D000936:Antigen-Antibody Complex; D001323:Autoantibodies