Enhanced response to enzyme replacement therapy in Pompe disease after the induction of immune tolerance. - Wikidata - wikimedia - TriplyDB

Enhanced response to enzyme replacement therapy in Pompe disease after the induction of immune tolerance.

Enhanced response to enzyme replacement therapy in Pompe disease after the induction of immune tolerance.

http://www.wikidata.org/entity/Q36492202

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Enzyme replacement therapy for infantile-onset Pompe disease Targeted approaches to induce immune tolerance for Pompe disease therapy New insights into therapeutic options for Pompe disease Use of cardiac magnetic resonance imaging to evaluate cardiac structure, function and fibrosis in children with infantile Pompe disease on enzyme replacement therapy.Tolerance induction to cytoplasmic beta-galactosidase by hepatic AAV gene transfer: implications for antigen presentation and immunotoxicity Immunomodulatory gene therapy prevents antibody formation and lethal hypersensitivity reactions in murine pompe disease.Hepatic gene transfer as a means of tolerance induction to transgene products Hepatocyte-targeted HFE and TFR2 control hepcidin expression in mice.The role of hepatocyte hemojuvelin in the regulation of bone morphogenic protein-6 and hepcidin expression in vivo.Cell-Mediated Immunity to AAV Vectors, Evolving Concepts and Potential Solutions.Immunomodulatory gene therapy in lysosomal storage disorders Mapping the T helper cell response to acid α-glucosidase in Pompe mice Therapeutic approaches for lysosomal storage diseases The impact of antibodies on clinical outcomes in diseases treated with therapeutic protein: lessons learned from infantile Pompe disease.Development of Gene Transfer for Induction of Antigen-specific Tolerance.Enhanced efficacy from gene therapy in Pompe disease using coreceptor blockade Early treatment with alglucosidase alpha prolongs long-term survival of infants with Pompe disease Assessment of toxicity and biodistribution of recombinant AAV8 vector-mediated immunomodulatory gene therapy in mice with Pompe disease.Systemic administration of AAV8-α-galactosidase A induces humoral tolerance in nonhuman primates despite low hepatic expression Comparative impact of AAV and enzyme replacement therapy on respiratory and cardiac function in adult Pompe mice Preclinical Development of New Therapy for Glycogen Storage Diseases.Preclinical dose-finding study with a liver-tropic, recombinant AAV-2/8 vector in the mouse model of galactosialidosis.Toward reducing immunogenicity of enzyme replacement therapy: altering the specificity of human β-glucuronidase to compensate for α-iduronidase deficiency.Immunodominant liver-specific expression suppresses transgene-directed immune responses in murine pompe disease Oral delivery of Acid Alpha Glucosidase epitopes expressed in plant chloroplasts suppresses antibody formation in treatment of Pompe mice.Synergistic Efficacy from Gene Therapy with Coreceptor Blockade and a β2-Agonist in Murine Pompe Disease.Neutralizing antibodies to therapeutic enzymes: considerations for testing, prevention and treatment Adjunctive β2-agonists reverse neuromuscular involvement in murine Pompe disease.Copackaged AAV9 Vectors Promote Simultaneous Immune Tolerance and Phenotypic Correction of Pompe Disease.Deficiency in MyD88 Signaling Results in Decreased Antibody Responses to an Adeno-Associated Virus Vector in Murine Pompe Disease.Pre-existing Antibody: Biotherapeutic Modality-Based Review.Salmeterol enhances the cardiac response to gene therapy in Pompe disease.Antibody formation and mannose-6-phosphate receptor expression impact the efficacy of muscle-specific transgene expression in murine Pompe disease.Cross-reactive immunologic material status affects treatment outcomes in Pompe disease infants.Immunity to adeno-associated virus vectors in animals and humans: a continued challenge.Potential of AAV vectors in the treatment of metabolic disease.Therapeutic approaches in glycogen storage disease type II/Pompe Disease.A Modified Enzymatic Method for Measurement of Glycogen Content in Glycogen Storage Disease Type IV.Non-depleting anti-CD4 monoclonal antibody induces immune tolerance to ERT in a murine model of Pompe disease.Low-Dose Liver-Targeted Gene Therapy for Pompe Disease Enhances Therapeutic Efficacy of ERT via Immune Tolerance Induction.

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P2860

Enhanced response to enzyme replacement therapy in Pompe disease after the induction of immune tolerance.

http://www.wikidata.org/entity/Q36492202

description

2007 nî lūn-bûn

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Enhanced response to enzyme re ...... induction of immune tolerance.

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American Journal of Human Genetics

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Enhanced response to enzyme re ...... induction of immune tolerance.

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Andrew Bird

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Baodong Sun

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Dwight D Koeberl

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Priya S Kishnani

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Sarah P Young

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Y-T Chen

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P2860

Novel adeno-associated viruses from rhesus monkeys as vectors for human gene therapy

Clinical and metabolic correction of pompe disease by enzyme therapy in acid maltase-deficient quail

Recombinant human acid [alpha]-glucosidase: major clinical benefits in infantile-onset Pompe disease

Glycogen stored in skeletal but not in cardiac muscle in acid alpha-glucosidase mutant (Pompe) mice is highly resistant to transgene-encoded human enzyme

Targeted disruption of the acid alpha-glucosidase gene in mice causes an illness with critical features of both infantile and adult human glycogen storage disease type II

Successful transduction of liver in hemophilia by AAV-Factor IX and limitations imposed by the host immune response

Chinese hamster ovary cell-derived recombinant human acid alpha-glucosidase in infantile-onset Pompe disease.

Genetic fate of recombinant adeno-associated virus vector genomes in muscle

Successful readministration of adeno-associated virus vectors to the mouse lung requires transient immunosuppression during the initial exposure

Recombinant human acid alpha-glucosidase enzyme therapy for infantile glycogen storage disease type II: results of a phase I/II clinical trial.

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1042-1049

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81

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5921404

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17924344

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Enzyme replacement therapy

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2265658

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