A role for complement in transmissible spongiform encephalopathies

Nature Medicine

Volumn 7, Issue 4, 2001, Pages 410-411

  Cardone, F ^a   Pocchiari, M ^a  

^a ISTITUTO SUPERIORE DI SANITÀ   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

COMPLEMENT SYSTEM; DISEASE ASSOCIATION; DISEASE TRANSMISSION; IMMUNE SYSTEM; PATHOGENESIS; PRION DISEASE; PRIORITY JOURNAL; SHORT SURVEY;

ANIMALS; CATTLE; COMPLEMENT SYSTEM PROTEINS; CREUTZFELDT-JAKOB SYNDROME; ENCEPHALOPATHY, BOVINE SPONGIFORM; HUMANS; NERVOUS SYSTEM; PRION DISEASES;

EID: 0035048448     PISSN: 10788956     EISSN: None     Source Type: Journal    
DOI: 10.1038/86469     Document Type: Short Survey

References (16)

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7. Temporary depletion of complement component C3 or genetic deficiency of C1q significantly delays onset of scrapie
8. Prion diseases and the immune system
9. Prion protein and the transmissible spongiform encephalopathy diseases
10. The presence of complements in amyloid plaques of Creutzfeldt-Jakob disease and Gerstmann-Sträussler-Scheinker disease
11. The phantasmagoric immunology of transmissible spongiform encephalopathy
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13. Pathogenesis of mouse scrapie: Patterns of agent replication in different parts of the CNS following intraperitoneal infection
14. Evidence for an alternative direct route of access for the scrapie agent to the brain bypassing the spinal cord
15. Entry versus blockade of brain infection following oral or intraperitoneal scrapie administration: Role of prion protein expression in peripheral nerves and spleen
16. A novel erythroid-specific marker of transmissible spongiform encephalopathies