title: Scrapie pathogenesis in subclinically infected B-cell-deficient mice.
abstract: Prion infections can present without clinical manifestations. B-cell deficiency may be a model for subclinical transmissible spongiform encephalopathy, since it protects mice from disease upon intraperitoneal administration of scrapie prions; however, a proportion of B-cell-deficient mice accumulate protease-resistant prion protein in their brains. Here, we have characterized this subclinical disease. In addition, we have studied the possibility that a neurotoxic factor secreted by B cells may contribute to pathogenesis.
authors.affiliation: Institutes of Neuropathology, Department of Pathology, CH-8091 Zurich, Switzerland.
authors.forename: R
authors.initials: R
authors.lastname: Frigg
authors.forename: M A
authors.initials: MA
authors.lastname: Klein
authors.forename: I
authors.initials: I
authors.lastname: Hegyi
authors.forename: R M
authors.initials: RM
authors.lastname: Zinkernagel
authors.forename: A
authors.initials: A
authors.lastname: Aguzzi
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D015153:Blotting, Western; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D019286:Endopeptidase K / Q000378:metabolism; D051379:Mice; D018620:PrPSc Proteins / Q000032:analysis / Q000378:metabolism; D012608:Scrapie / Q000276:immunology / Q000473:pathology*
chemical_list: D018620:PrPSc Proteins; D019286:Endopeptidase K