Mechanisms of Schwann cell damage in inflammatory neuropathy.
Inflammatory demyelination of nerve in Guillain-Barré syndrome is triggered in most patients by prior infection with one of a series of organisms, including Campylobacter jejuni. The resulting inflammatory cascade, involving T cells, macrophages, complement, and cytokines, disrupts physiologic function of the peripheral nerve in part by targeting Schwann cells, the multipotential glial cells that synthesize multilamellar, compacted myelin and secrete growth factors. In vitro evidence suggests that the Schwann cell may itself be able to modulate the cascade by serving as an antigen-presenting cell and by producing cytokines and other acute-phase reactants.
Koski
C L
CL
Department of Neurology, University of Maryland School of Medicine, Baltimore 21201-1595, USA.
D000818:Animals; D017951:Antigen Presentation; D002169:Campylobacter Infections / Q000150:complications; D003165:Complement System Proteins / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D006801:Humans; D007239:Infections / Q000150:complications; D008264:Macrophages / Q000276:immunology; D009443:Neuritis / Q000150:complications / Q000276:immunology; D010525:Peripheral Nerves / Q000276:immunology / Q000473:pathology; D011129:Polyradiculoneuropathy / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D051381:Rats; D012583:Schwann Cells / Q000276:immunology* / Q000473:pathology* / Q000502:physiology; D013601:T-Lymphocytes / Q000276:immunology
D016207:Cytokines; D003165:Complement System Proteins