Guillain-Barré as an autoimmune disease.
Guillain-Barré syndrome (GBS) entails a demyelinating process of the peripheral nervous system. The etiopathogenesis of the syndrome is still a matter of debate although considerable progress has been accomplished in the recent years. Abundant evidence has been put forward so as to support the role of the immune system in initiating and perpetuating the ongoing damage culminating in the emergence of the clinically overt syndrome. As such, data on the involvement of the humoral immune pathways add to the information already presented with regard to cell-mediated mechanisms participating in disruption of peripheral nerve. The following review will focus on the current knowledge of these complex mechanisms and the relative significance of each in the pathogenesis of GBS.
Shoenfeld
Y
Y
Department of Medicine 'B', Sheba Medical Center, Tel Hashomer, Israel.
George
J
J
Peter
J B
JB
D000818:Animals; D001323:Autoantibodies; D001324:Autoantigens; D001327:Autoimmune Diseases / Q000209:etiology* / Q000628:therapy; D003167:Complement Activation; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D006801:Humans; D007116:Immunization, Passive; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007239:Infections / Q000150:complications; D008285:Major Histocompatibility Complex; D008954:Models, Biological; D009444:Neuritis, Autoimmune, Experimental / Q000209:etiology / Q000276:immunology; D010956:Plasmapheresis; D011129:Polyradiculoneuropathy / Q000209:etiology* / Q000276:immunology* / Q000628:therapy; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies; D001324:Autoantigens; D016207:Cytokines; D016756:Immunoglobulins, Intravenous