Immunomodulatory, liver depot gene therapy for Pompe disease.


Journal

Cellular immunology
ISSN: 1090-2163
Titre abrégé: Cell Immunol
Pays: Netherlands
ID NLM: 1246405

Informations de publication

Date de publication:
08 2019
Historique:
received: 01 11 2017
revised: 15 12 2017
accepted: 27 12 2017
pubmed: 4 1 2018
medline: 7 5 2020
entrez: 4 1 2018
Statut: ppublish

Résumé

Pompe disease is caused by mutations in acid alpha glucosidase (GAA) that causes accumulation of lysosomal glycogen affecting the heart and skeletal muscles, and can be fatal. Enzyme replacement therapy (ERT) with recombinant human GAA (rhGAA) improves muscle function by reducing glycogen accumulation. Limitations of ERT include a short half-life and the formation of antibodies that result in reduced efficacy. By harnessing the immune tolerance induction properties of the liver, liver-targeted gene delivery (with an adeno-associated virus vector containing a liver specific promoter), suppresses immunity against the GAA introduced by gene therapy. This induces immune tolerance to rhGAA by activating regulatory T cells and simultaneously, corrects GAA deficiency. Potentially, liver-targeted gene therapy can be performed once with lasting effects, by administering a relatively low dose of an adeno-associated virus type 8 vector to replace and induce immune tolerance to GAA.

Identifiants

pubmed: 29295737
pii: S0008-8749(17)30238-1
doi: 10.1016/j.cellimm.2017.12.011
pmc: PMC6026080
mid: NIHMS931846
pii:
doi:

Substances chimiques

GAA protein, human EC 3.2.1.20
alpha-Glucosidases EC 3.2.1.20

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

103737

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR065873
Pays : United States
Organisme : NIAMS NIH HHS
ID : U01 AR071693
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD054795
Pays : United States

Informations de copyright

Copyright © 2018 Elsevier Inc. All rights reserved.

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Auteurs

J E Bond (JE)

Clinical and Translational Science Institute, Duke University, Durham, NC, USA.

P S Kishnani (PS)

Division of Medical Genetics, Department of Pediatrics, Duke University Medical School, Durham, NC, USA.

D D Koeberl (DD)

Division of Medical Genetics, Department of Pediatrics, Duke University Medical School, Durham, NC, USA; Molecular Genetics and Microbiology, Duke University, Durham, NC, USA. Electronic address: koebe001@mc.duke.edu.

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