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spelling todo:paper_1170229X_v12_n1_p29_Chernajovsky2023-10-03T16:08:10Z Gene therapy for rheumatoid arthritis. Theoretical considerations Chernajovsky, Y. Annenkov, A. Herman, C. Triantaphyllopoulos, K. Gould, D. Dreja, H. Moyes, S.P. Croxford, J.L. Mageed, R.A. Podhajcer, O.L. Baker, D. antirheumatic agent antisense oligonucleotide cytokine cytokine receptor immunoglobulin enhancer binding protein immunoglobulin fragment interleukin 1 interleukin 1 receptor blocking agent interleukin 10 plasmid DNA transforming growth factor beta1 tumor necrosis factor alpha tumor necrosis factor alpha antibody virus vector cell type clinical trial complement system gene targeting gene therapy human major clinical study mediator meta analysis priority journal review rheumatoid arthritis Arthritis, Rheumatoid Gene Therapy Genetic Vectors Humans Current understanding of the pathogenesis of rheumatoid arthritis has provided evidence that therapeutic benefit can be achieved by using antagonists targeted to the inflammatory cytokines involved, mainly tumour necrosis factor-α and interleukin-1. Gene delivery of antagonists, which can inhibit the production or action of these cytokines and other mediators, has been achieved in experimental animal models. This new method of delivery can produce therapeutic effects at lower concentrations and in a local environment, overcoming the adverse effects that often accompany protein therapy. However, several technological and biological restraints preclude the immediate adaptation of this method to human treatment. Based on the experimental evidence, possible target therapeutic genes, cell types and vector systems that could be used are discussed in this article. Fil:Podhajcer, O.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_1170229X_v12_n1_p29_Chernajovsky
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic antirheumatic agent
antisense oligonucleotide
cytokine
cytokine receptor
immunoglobulin enhancer binding protein
immunoglobulin fragment
interleukin 1
interleukin 1 receptor blocking agent
interleukin 10
plasmid DNA
transforming growth factor beta1
tumor necrosis factor alpha
tumor necrosis factor alpha antibody
virus vector
cell type
clinical trial
complement system
gene targeting
gene therapy
human
major clinical study
mediator
meta analysis
priority journal
review
rheumatoid arthritis
Arthritis, Rheumatoid
Gene Therapy
Genetic Vectors
Humans
spellingShingle antirheumatic agent
antisense oligonucleotide
cytokine
cytokine receptor
immunoglobulin enhancer binding protein
immunoglobulin fragment
interleukin 1
interleukin 1 receptor blocking agent
interleukin 10
plasmid DNA
transforming growth factor beta1
tumor necrosis factor alpha
tumor necrosis factor alpha antibody
virus vector
cell type
clinical trial
complement system
gene targeting
gene therapy
human
major clinical study
mediator
meta analysis
priority journal
review
rheumatoid arthritis
Arthritis, Rheumatoid
Gene Therapy
Genetic Vectors
Humans
Chernajovsky, Y.
Annenkov, A.
Herman, C.
Triantaphyllopoulos, K.
Gould, D.
Dreja, H.
Moyes, S.P.
Croxford, J.L.
Mageed, R.A.
Podhajcer, O.L.
Baker, D.
Gene therapy for rheumatoid arthritis. Theoretical considerations
topic_facet antirheumatic agent
antisense oligonucleotide
cytokine
cytokine receptor
immunoglobulin enhancer binding protein
immunoglobulin fragment
interleukin 1
interleukin 1 receptor blocking agent
interleukin 10
plasmid DNA
transforming growth factor beta1
tumor necrosis factor alpha
tumor necrosis factor alpha antibody
virus vector
cell type
clinical trial
complement system
gene targeting
gene therapy
human
major clinical study
mediator
meta analysis
priority journal
review
rheumatoid arthritis
Arthritis, Rheumatoid
Gene Therapy
Genetic Vectors
Humans
description Current understanding of the pathogenesis of rheumatoid arthritis has provided evidence that therapeutic benefit can be achieved by using antagonists targeted to the inflammatory cytokines involved, mainly tumour necrosis factor-α and interleukin-1. Gene delivery of antagonists, which can inhibit the production or action of these cytokines and other mediators, has been achieved in experimental animal models. This new method of delivery can produce therapeutic effects at lower concentrations and in a local environment, overcoming the adverse effects that often accompany protein therapy. However, several technological and biological restraints preclude the immediate adaptation of this method to human treatment. Based on the experimental evidence, possible target therapeutic genes, cell types and vector systems that could be used are discussed in this article.
format JOUR
author Chernajovsky, Y.
Annenkov, A.
Herman, C.
Triantaphyllopoulos, K.
Gould, D.
Dreja, H.
Moyes, S.P.
Croxford, J.L.
Mageed, R.A.
Podhajcer, O.L.
Baker, D.
author_facet Chernajovsky, Y.
Annenkov, A.
Herman, C.
Triantaphyllopoulos, K.
Gould, D.
Dreja, H.
Moyes, S.P.
Croxford, J.L.
Mageed, R.A.
Podhajcer, O.L.
Baker, D.
author_sort Chernajovsky, Y.
title Gene therapy for rheumatoid arthritis. Theoretical considerations
title_short Gene therapy for rheumatoid arthritis. Theoretical considerations
title_full Gene therapy for rheumatoid arthritis. Theoretical considerations
title_fullStr Gene therapy for rheumatoid arthritis. Theoretical considerations
title_full_unstemmed Gene therapy for rheumatoid arthritis. Theoretical considerations
title_sort gene therapy for rheumatoid arthritis. theoretical considerations
url http://hdl.handle.net/20.500.12110/paper_1170229X_v12_n1_p29_Chernajovsky
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AT triantaphyllopoulosk genetherapyforrheumatoidarthritistheoreticalconsiderations
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AT podhajcerol genetherapyforrheumatoidarthritistheoreticalconsiderations
AT bakerd genetherapyforrheumatoidarthritistheoreticalconsiderations
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