The University of Southampton
University of Southampton Institutional Repository

PD-1 deficiency is not sufficient to induce myeloid mobilization to the brain or alter the inflammatory profile during chronic neurodegeneration

PD-1 deficiency is not sufficient to induce myeloid mobilization to the brain or alter the inflammatory profile during chronic neurodegeneration
PD-1 deficiency is not sufficient to induce myeloid mobilization to the brain or alter the inflammatory profile during chronic neurodegeneration
Chronic inflammation is a major driver of neurodegenerative disease and immune regulatory pathways could be potential targets for therapeutic intervention. Recently, Programmed cell death-1 (PD-1) immune checkpoint inhibition has been proposed to mount an IFN-γ-dependent systemic immune response, leading to the recruitment of peripheral myeloid cells to the brain and neuropathological and functional improvements in mice with Alzheimer’s disease- like β-amyloid pathology. Here we investigate the impact of PD-1 deficiency on murine prion disease (ME7 strain), a model of chronic neurodegeneration. Although PD-1 was found to be increased in the brain of prion mice, the absence of PD-1 did not cause myeloid cell infiltration into the brain or major changes in the inflammatory profile. However, we observed a slight exacerbation of the behavioural phenotype of ME7 mice upon PD-1 deficiency. These results do not support the possibility of using immune checkpoint blockade as a therapeutic strategy in neurodegenerative disease.
0889-1591
Obst, Juliane
0c499ee6-0290-4792-8c99-049e05332227
Mancuso, Renzo
05786562-a993-4e37-926e-3c1fcf50b36d
Simon, Emilie
22a3ee84-1834-4038-91cb-15d6163b1c56
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5
Obst, Juliane
0c499ee6-0290-4792-8c99-049e05332227
Mancuso, Renzo
05786562-a993-4e37-926e-3c1fcf50b36d
Simon, Emilie
22a3ee84-1834-4038-91cb-15d6163b1c56
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5

Obst, Juliane, Mancuso, Renzo, Simon, Emilie and Gomez-Nicola, Diego (2018) PD-1 deficiency is not sufficient to induce myeloid mobilization to the brain or alter the inflammatory profile during chronic neurodegeneration. Brain, Behavior and Immunity. (doi:10.1016/j.bbi.2018.08.006).

Record type: Article

Abstract

Chronic inflammation is a major driver of neurodegenerative disease and immune regulatory pathways could be potential targets for therapeutic intervention. Recently, Programmed cell death-1 (PD-1) immune checkpoint inhibition has been proposed to mount an IFN-γ-dependent systemic immune response, leading to the recruitment of peripheral myeloid cells to the brain and neuropathological and functional improvements in mice with Alzheimer’s disease- like β-amyloid pathology. Here we investigate the impact of PD-1 deficiency on murine prion disease (ME7 strain), a model of chronic neurodegeneration. Although PD-1 was found to be increased in the brain of prion mice, the absence of PD-1 did not cause myeloid cell infiltration into the brain or major changes in the inflammatory profile. However, we observed a slight exacerbation of the behavioural phenotype of ME7 mice upon PD-1 deficiency. These results do not support the possibility of using immune checkpoint blockade as a therapeutic strategy in neurodegenerative disease.

Text
1-s2.0-S0889159118304161-main - Accepted Manuscript
Available under License Creative Commons Attribution.
Download (1MB)

More information

Accepted/In Press date: 3 August 2018
e-pub ahead of print date: 4 August 2018

Identifiers

Local EPrints ID: 422952
URI: http://eprints.soton.ac.uk/id/eprint/422952
ISSN: 0889-1591
PURE UUID: 61a50981-c60a-42ea-8d71-dc95799a9347
ORCID for Diego Gomez-Nicola: ORCID iD orcid.org/0000-0002-5316-2682

Catalogue record

Date deposited: 08 Aug 2018 16:30
Last modified: 16 Mar 2024 04:04

Export record

Altmetrics

Contributors

Author: Juliane Obst
Author: Renzo Mancuso
Author: Emilie Simon

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×