RGD Reference Report - Prion pathogenesis is unaltered following down-regulation of SIGN-R1. - Rat Genome Database

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Prion pathogenesis is unaltered following down-regulation of SIGN-R1.

Authors: Bradford, Barry M  Brown, Karen L  Mabbott, Neil A 
Citation: Bradford BM, etal., Virology. 2016 Oct;497:337-345. doi: 10.1016/j.virol.2016.08.005. Epub 2016 Aug 11.
RGD ID: 40400758
Pubmed: PMID:27522473   (View Abstract at PubMed)
PMCID: PMC5031137   (View Article at PubMed Central)
DOI: DOI:10.1016/j.virol.2016.08.005   (Journal Full-text)

Prion diseases are infectious neurodegenerative disorders characterised by accumulations of abnormal prion glycoprotein in affected tissues. Following peripheral exposure, many prion strains replicate upon follicular dendritic cells (FDC) in lymphoid tissues before infecting the brain. An intact splenic marginal zone is important for the efficient delivery of prions to FDC. The marginal zone contains a ring of specific intercellular adhesion molecule-3-grabbing non-integrin related 1 (SIGN-R1)-expressing macrophages. This lectin binds dextran and capsular pneumococcal polysaccharides, and also enhances the clearance of apoptotic cells via interactions with complement components. Since prions are acquired as complement-opsonized complexes we determined the role of SIGN-R1 in disease pathogenesis. We show that transient down-regulation of SIGN-R1 prior to intravenous prion exposure had no effect on the early accumulation of prions upon splenic FDC or their subsequent spread to the brain. Thus, SIGN-R1 expression by marginal zone macrophages is not rate-limiting for peripheral prion disease pathogenesis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Cd209aRatscrapie  ISOCd209a (Mus musculus) RGD 
Cd209aMousescrapie  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cd209a  (CD209a molecule)

Genes (Mus musculus)
Cd209a  (CD209a antigen)


Additional Information