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CpG and LPS can interfere negatively with prion clearance in macrophage and microglial cells.
FEBS J. 274, 5834-5844 (2007)
Cells of the innate immune system play important roles in the progression of prion disease after peripheral infection. It has been found in vivo and in vitro that the expression of the cellular prion protein (PrP(c)) is up-regulated on stimulation of immune cells, also indicating the functional importance of PrP(c) in the immune system. The aim of our study was to investigate the impact of cytosine-phosphate-guanosine- and lipopolysaccharide-induced PrP(c) up-regulation on the uptake and processing of the pathological prion protein (PrP(Sc)) in phagocytic innate immune cells. For this purpose, we challenged the macrophage cell line J774, the microglial cell line BV-2 and primary bone marrow-derived macrophages in a resting or stimulated state with various prion strains, and monitored the uptake and clearance of PrP(Sc). Interestingly, stimulation led either to a transient increase in the level of PrP(Sc) relative to unstimulated cells or to a decelerated degradation of PrP(Sc). These features were dependent on cell type and prion strain. Our data indicate that the stimulation of innate immune cells may be able to support transient prion propagation, possibly explained by an increased PrP(c) cell surface expression in stimulated cells. We suggest that stimulation of innate immune cells can lead to an imbalance between the propagation and degradation of PrP(Sc).
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
3.033
0.000
18
14
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
innate immunity; prion; prion clearance; PAMP; toll-like receptor
Sprache
englisch
Veröffentlichungsjahr
2007
HGF-Berichtsjahr
0
ISSN (print) / ISBN
1742-464X
e-ISSN
1742-4658
Zeitschrift
FEBS Journal, The
Quellenangaben
Band: 274,
Heft: 22,
Seiten: 5834-5844
Verlag
Wiley
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Molecular Immunology (IMI)
PSP-Element(e)
G-501700-003
PubMed ID
17944938
WOS ID
000250586500008
Erfassungsdatum
2007-11-26