D. Serra

发表

Depleting regulatory T cells with arginine-rich, cell-penetrating, peptide-conjugated morpholino oligomer targeting FOXP3 inhibits regulatory T-cell function

P. Iversen, K. Aird, M. Morse, 2011, Cancer Gene Therapy.

Persistence of an [E1-, polymerase-] adenovirus vector despite transduction of a neoantigen into immune-competent mice.

A. Amalfitano, H. Hu, D. Serra, 1999, Human gene therapy.

Applications of adenoviral vector-mediated gene transfer in cardiovascular research.

A. Amalfitano, D. Serra, Fang Xu, 2006, Methods in molecular medicine.

Production and Characterization of Improved Adenovirus Vectors with the E1, E2b, and E3 Genes Deleted

J. Chamberlain, A. Amalfitano, M. Hauser, 1998, Journal of Virology.

Fully deleted adenovirus persistently expressing GAA accomplishes long-term skeletal muscle glycogen correction in tolerant and nontolerant GSD-II mice.

A. Kiang, Z. Hartman, A. Amalfitano, 2006, Molecular therapy : the journal of the American Society of Gene Therapy.

Glycogen storage in multiple muscles of old GSD‐II mice can be rapidly cleared after a single intravenous injection with a modified adenoviral vector expressing hGAA

Yuan-Tsong Chen, A. Amalfitano, E. Ding, 2005, The journal of gene medicine.

Improved efficacy of gene therapy approaches for Pompe disease using a new, immune-deficient GSD-II mouse model

A. Amalfitano, J. Dai, E. Ding, 2004, Gene Therapy.

Efficacy of gene therapy for a prototypical lysosomal storage disease (GSD-II) is critically dependent on vector dose, transgene promoter, and the tissues targeted for vector transduction.

Yuan-Tsong Chen, A. Amalfitano, B. Hodges, 2002, Molecular therapy : the journal of the American Society of Gene Therapy.

Long-term efficacy after [E1-, polymerase-] adenovirus-mediated transfer of human acid-alpha-glucosidase gene into glycogen storage disease type II knockout mice.

A. Amalfitano, Y. T. Chen, A. McVie-Wylie, 2001, Human gene therapy.

Replication-attenuated Human Adenoviral Type 4 vectors elicit capsid dependent enhanced innate immune responses that are partially dependent upon interactions with the complement system.

Z. Hartman, A. Amalfitano, D. Appledorn, 2008, Virology.

Multiple innate inflammatory responses induced after systemic adenovirus vector delivery depend on a functional complement system.

A. Kiang, M. Frank, Z. Hartman, 2006, Molecular therapy : the journal of the American Society of Gene Therapy.

Production and Characterization of Improved Adenovirus Vectors with the E 1 , E 2 b , and E 3 Genes Deleted

J. Chamberlain, A. Amalfitano, M. Hauser, 1998 .

Adenovirus Vectors with the 100K Gene Deleted and Their Potential for Multiple Gene Therapy Applications

A. Amalfitano, B. Hodges, E. Ding, 2001, Journal of Virology.

Liver toxicities typically induced by first-generation adenoviral vectors can be reduced by use of E1, E2b-deleted adenoviral vectors.

A. Amalfitano, B. Hodges, E. Ding, 2003, Human gene therapy.

Multiply deleted [E1, polymerase‐, and pTP‐] adenovirus vector persists despite deletion of the preterminal protein

J. Chamberlain, A. Amalfitano, B. Hodges, 2000, The journal of gene medicine.

Strain-specific rate of shutdown of CMV enhancer activity in murine liver confirmed by use of persistent [E1(-), E2b(-)] adenoviral vectors.

A. Amalfitano, B. Hodges, E. Ding, 2004, Virology.

Depletion of human regulatory T cells specifically enhances antigen-specific immune responses to cancer vaccines.

D. Niedzwiecki, H. Lyerly, M. Morse, 2008, Blood.

Adenovirus Infection Triggers a Rapid, MyD88-Regulated Transcriptome Response Critical to Acute-Phase and Adaptive Immune Responses In Vivo

A. Kiang, Z. Hartman, A. Amalfitano, 2006, Journal of Virology.

Detailed analysis of cytomegalovirus (CMV)-specific T cells expanded for adoptive immunotherapy of CMV infection following allogeneic stem cell transplantation for malignant disease.

Y. Tanaka, D. Niedzwiecki, D. Rizzieri, 2008, Cytotherapy.

Recombinant adenovirus vectors activate the alternative complement pathway, leading to the binding of human complement protein C3 independent of anti-ad antibodies.

M. Frank, A. Amalfitano, Haixiang Jiang, 2004, Molecular therapy : the journal of the American Society of Gene Therapy.

Multiple muscles in the AMD quail can be “cross‐corrected” of pathologic glycogen accumulation after intravenous injection of an [E1‐, polymerase‐] adenovirus vector encoding human acid‐α‐glucosidase

A. Amalfitano, T. Kikuchi, M. Mizutani, 2003, The journal of gene medicine.

Replication-attenuated Human Adenoviral Type 4 vectors elicit capsid dependent enhanced innate immune responses that are partially dependent upon interactions with the complement system.

Z. Hartman, A. Amalfitano, D. Appledorn, 2008, Virology.