Amyloid-β specific regulatory T cells attenuate Alzheimer's disease pathobiology in APP/PS1 mice.

Alzheimer’s disease Amyloid beta Antigen specific Immunotherapy T cell receptor Treg cell therapy

Journal

Molecular neurodegeneration
ISSN: 1750-1326
Titre abrégé: Mol Neurodegener
Pays: England
ID NLM: 101266600

Informations de publication

Date de publication:
18 Dec 2023
Historique:
received: 29 05 2023
accepted: 04 12 2023
medline: 19 12 2023
pubmed: 19 12 2023
entrez: 19 12 2023
Statut: epublish

Résumé

Regulatory T cells (Tregs) maintain immune tolerance. While Treg-mediated neuroprotective activities are now well-accepted, the lack of defined antigen specificity limits their therapeutic potential. This is notable for neurodegenerative diseases where cell access to injured brain regions is required for disease-specific therapeutic targeting and improved outcomes. To address this need, amyloid-beta (Aβ) antigen specificity was conferred to Treg responses by engineering the T cell receptor (TCR) specific for Aβ (TCR TCR TCR TCR

Sections du résumé

BACKGROUND BACKGROUND
Regulatory T cells (Tregs) maintain immune tolerance. While Treg-mediated neuroprotective activities are now well-accepted, the lack of defined antigen specificity limits their therapeutic potential. This is notable for neurodegenerative diseases where cell access to injured brain regions is required for disease-specific therapeutic targeting and improved outcomes. To address this need, amyloid-beta (Aβ) antigen specificity was conferred to Treg responses by engineering the T cell receptor (TCR) specific for Aβ (TCR
METHODS METHODS
TCR
RESULTS RESULTS
TCR
CONCLUSIONS CONCLUSIONS
TCR

Identifiants

pubmed: 38111016
doi: 10.1186/s13024-023-00692-7
pii: 10.1186/s13024-023-00692-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

97

Subventions

Organisme : NINDS NIH HHS
ID : 2R01 NS034239
Pays : United States

Informations de copyright

© 2023. The Author(s).

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Auteurs

Pravin Yeapuri (P)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Jatin Machhi (J)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Yaman Lu (Y)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Mai Mohamed Abdelmoaty (MM)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Rana Kadry (R)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Milankumar Patel (M)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Shaurav Bhattarai (S)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Eugene Lu (E)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Krista L Namminga (KL)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Katherine E Olson (KE)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Emma G Foster (EG)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

R Lee Mosley (RL)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA.

Howard E Gendelman (HE)

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, USA. hegendel@unmc.edu.

Classifications MeSH