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Atypical inflammation in the central nervous system in prion disease

Record type: Article

The inflammatory response in prion diseases is dominated by microglial activation. Contrary to their profile in vitro none of the pro-inflammatory cytokines interleukin-1[beta], interleukin-6, or tumour necrosis factor-[alpha] are significantly upregulated in the ME7 model of prion disease. However, two major inflammatory mediators are elevated: transforming growth factor-[beta]1 and prostaglandin E2. This cytokine profile is the same as that reported for macrophages during phagocytosis of apoptotic cells and indeed transforming growth factor-[beta]1 and prostaglandin E2 are responsible for the downregulated phenotype of these macrophages. Transforming growth factor-[beta]1 may also have roles in extracellular matrix deposition and in amyloidogenesis and may play a direct role in disease pathogenesis. There is also now evidence to suggest that a peripheral infection, and its consequent systemic cytokine expression, may drive central nervous system cytokine expression and perhaps exacerbate disease.

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Citation

Perry, VH., Cunningham, C. and Boche, D. (2002) Atypical inflammation in the central nervous system in prion disease Current Opinion in Neurology, 15, (3), pp. 349-354.

More information

Published date: June 2002

Identifiers

Local EPrints ID: 27683
URI: http://eprints.soton.ac.uk/id/eprint/27683
ISSN: 1350-7540
PURE UUID: 064669c4-f747-46b8-8a68-7972e00660f8
ORCID for D. Boche: ORCID iD orcid.org/0000-0002-5884-130X

Catalogue record

Date deposited: 25 Apr 2006
Last modified: 17 Jul 2017 16:04

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