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Prp expression in b lymphocytes is not required for prion neuroinvasion

Academic Article
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Overview

authors

  • Klein, M. A.
  • Frigg, R.
  • Raeber, A. J.
  • Flechsig, E.
  • Hegyi, I.
  • Zinkernagel, R. M.
  • Weissmann, Charles
  • Aguzzi, A.

publication date

  • December 1998

journal

  • Nature Medicine  Journal

abstract

  • 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.

subject areas

  • Animals
  • B-Lymphocytes
  • Biomarkers
  • Cattle
  • Central Nervous System
  • Encephalopathy, Bovine Spongiform
  • Homeodomain Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, SCID
  • Molecular Weight
  • Peripheral Nervous System
  • PrPSc Proteins
  • Prion Diseases
  • Prions
  • Virus Replication
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Identity

International Standard Serial Number (ISSN)

  • 1078-8956

Digital Object Identifier (DOI)

  • 10.1038/4022

PubMed ID

  • 9846583
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Additional Document Info

start page

  • 1429

end page

  • 1433

volume

  • 4

issue

  • 12

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