Abstract
rAAV-mediated gene transfer in skeletal muscle of large animal models can sustain long-term expression of transgene, but when applied to genetic diseases, the newly expressed therapeutic protein often induces a deleterious immune response. We investigated whether such immune response could be prevented by treatment with a mutant form of CTLA4Ig with higher affinity for B7 molecules (LEA29Y), known to induce potent immunosuppression and currently used, in its recombinant form (Belatacept®), in phase II/ III clinical development.
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