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Impaired prion replication in spleens of mice lacking functional follicular dendritic cells.


Montrasio, F; Frigg, R; Glatzel, M; Klein, M A; Mackay, F; Aguzzi, A; Weissmann, C (2000). Impaired prion replication in spleens of mice lacking functional follicular dendritic cells. Science, 288(5469):1257-1259.

Abstract

In scrapie-infected mice, prions are found associated with splenic but not circulating B and T lymphocytes and in the stroma, which contains follicular dendritic cells (FDCs). Formation and maintenance of mature FDCs require the presence of B cells expressing membrane-bound lymphotoxin-alpha/beta. Treatment of mice with soluble lymphotoxin-beta receptor results in the disappearance of mature FDCs from the spleen. We show that this treatment abolishes splenic prion accumulation and retards neuroinvasion after intraperitoneal scrapie inoculation. These data provide evidence that FDCs are the principal sites for prion replication in the spleen.

In scrapie-infected mice, prions are found associated with splenic but not circulating B and T lymphocytes and in the stroma, which contains follicular dendritic cells (FDCs). Formation and maintenance of mature FDCs require the presence of B cells expressing membrane-bound lymphotoxin-alpha/beta. Treatment of mice with soluble lymphotoxin-beta receptor results in the disappearance of mature FDCs from the spleen. We show that this treatment abolishes splenic prion accumulation and retards neuroinvasion after intraperitoneal scrapie inoculation. These data provide evidence that FDCs are the principal sites for prion replication in the spleen.

Citations

258 citations in Web of Science®
278 citations in Scopus®
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Additional indexing

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
Language:English
Date:19 May 2000
Deposited On:11 Feb 2008 12:26
Last Modified:05 Apr 2016 12:21
Publisher:American Association for the Advancement of Science (AAAS)
ISSN:0036-8075
Publisher DOI:10.1126/science.288.5469.1257
PubMed ID:10818004

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