The immunobiology of TSE diseases

Journal of General Virology

Volumn 82, Issue 10, 2001, Pages 2307-2318

  Mabbott, N A ^a   Bruce, M E ^a  

^a INSTITUTE FOR ANIMAL HEALTH   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; B LYMPHOCYTE; CHIMERA; COMPLEMENT ACTIVATION; CONTROLLED STUDY; DENDRITIC CELL; DISEASE TRANSMISSION; IMMUNOBIOLOGY; INCUBATION TIME; LYMPHOID TISSUE; MACROPHAGE; MOLECULAR INTERACTION; MOUSE; NONHUMAN; PATHOGENESIS; PRION DISEASE; PRIORITY JOURNAL; REVIEW; SPLEEN; T LYMPHOCYTE;

EID: 0034796073     PISSN: 00221317     EISSN: None     Source Type: Journal    
DOI: 10.1099/0022-1317-82-10-2307     Document Type: Review

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12. The cellular prion protein binds copper in vivo
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15. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent
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19. Cellular isoform of the scrapie agent protein participates in lymphocyte activation
20. Cytokine regulation of secondary lymphoid organ development
21. + currents
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57. Normal cellular prion protein is preferentially expressed on subpopulations of murine hemopoietic cells
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60. Tumor necrosis factor-alpha-deficient, but not interleukin-6-deficient, mice resist peripheral infection with scrapie
61. Temporary depletion of complement component C3 or genetic deficiency of C1q significantly delays onset of scrapie
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65. Turning off follicular dendritic cells
66. 129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal
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72. B-lymphocyte-restricted expression of the prion protein does not enable prion replication in PrP knockout mice
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