Klein, M A; Frigg, R; Raeber, A J; Flechsig, E; Hegyi, I; Zinkernagel, R M; Weissmann, C; Aguzzi, A (1998). PrP expression in B lymphocytes is not required for prion neuroinvasion. Nature Medicine, 4(12):1429-1433.
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Prion diseases are typically initiated by infection of peripheral sites, as in the case of bovine spongiform encephalopathy, new variant Creutzfeldt-Jakob disease, kuru and most cases of iatrogenic Creutzfeldt-Jakob disease. In mouse scrapie, prion infectivity accumulates in lymphoid organs, and the absence of mature B lymphocytes prevents peripherally administered prions from inducing central nervous system disease. We have now assessed whether expression of the cellular prion protein, PrPc, is required for B lymphocytes to mediate neuroinvasion. We found that repopulation of SCID and Rag-1(-/-) mice with fetal liver cells from either PrP-expressing or PrP-deficient mice and from T-cell deficient mice, but not from B-cell deficient mice, is equally efficient in restoring neuroinvasion after intraperitoneal inoculation of scrapie prions. These results indicate that cells whose maturation depends on B cells or their products, such as follicular dendritic cells, may enhance neuroinvasion. Alternatively, B cells may transport prions to the nervous system by a PrP-independent mechanism.
|Item Type:||Journal Article, refereed|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|Dewey Decimal Classification:||570 Life sciences; biology
610 Medicine & health
|Date:||1 December 1998|
|Deposited On:||11 Feb 2008 12:25|
|Last Modified:||05 Apr 2016 12:20|
|Publisher:||Nature Publishing Group|
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