Gene therapy for rheumatoid arthritis. Theoretical considerations

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 th...

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Autor principal: Chernajovsky, Y.
Otros Autores: Annenkov, A., Herman, C., Triantaphyllopoulos, K., Gould, D., Dreja, H., Moyes, S.P, Croxford, J.L, Mageed, R.A, Podhajcer, O.L, Baker, D.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1998
Acceso en línea:Registro en Scopus
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100 1 |a Chernajovsky, Y. 
245 1 0 |a Gene therapy for rheumatoid arthritis. Theoretical considerations 
260 |c 1998 
270 1 0 |m Chernajovsky, Y.; Molecular Biology Laboratory, Kennedy Institute of Rheumatology, 1 Aspenlea Road, London W6 8LH, United Kingdom; email: ychernaj@gmp.mrc.ac.uk 
506 |2 openaire  |e Política editorial 
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504 |a Roivainen, A., Jalava, J., Pirila, L., H-ras oncogene point mutations in arthritic synovium (1996) Arthritis Rheum, 40, pp. 1636-1643 
504 |a Berenblum, I., The mechanisms of carcinogenesis - A study of the significance of co-carcinogenic action and related phenomena (1981) Cancer J Clinicians, 31, pp. 241-253 
504 |a Baragi, V.M., Renkiewicz, R.R., Jordan, H., Transplantation of transduced chondrocytes protects articular cartilage from interleukin 1-induced extracellular matrix degradation (1995) J Clin Invest, 96, pp. 2454-2460 
520 3 |a 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.  |l eng 
536 |a Detalles de la financiación: Mineralogical Society of Great Britain and Ireland 
536 |a Detalles de la financiación: Fundación Antorchas 
536 |a Detalles de la financiación: Wellcome Trust 
536 |a Detalles de la financiación: We would like to thank Drs Boissier and Makarov for their personal communications. Part of this work has been supported by the UK Arthritis and Rheumatism Council, the Multiple Sclerosis Society of Great Britain and Northern Ireland, The Wellcome Trust, The Nuffield Foundation and The British Council, and the Fundación Antorchas in Argentina. 
593 |a Molecular Biology Laboratory, Kennedy Institute of Rheumatology, London, United Kingdom 
593 |a Clinical Immunology Division, Kennedy Institute of Rheumatology, London, United Kingdom 
593 |a Institute of Ophthalmology, University College London, London, United Kingdom 
593 |a Fundación Campomar, Fac. de Ciencias Exactas y Naturales, University of Buenos Aires, Buenos Aires, Argentina 
593 |a Molecular Biology Laboratory, Kennedy Institute of Rheumatology, 1 Aspenlea Road, Hammersmith, London W6 8LH, United Kingdom 
690 1 0 |a ANTIRHEUMATIC AGENT 
690 1 0 |a ANTISENSE OLIGONUCLEOTIDE 
690 1 0 |a CYTOKINE 
690 1 0 |a CYTOKINE RECEPTOR 
690 1 0 |a IMMUNOGLOBULIN ENHANCER BINDING PROTEIN 
690 1 0 |a IMMUNOGLOBULIN FRAGMENT 
690 1 0 |a INTERLEUKIN 1 
690 1 0 |a INTERLEUKIN 1 RECEPTOR BLOCKING AGENT 
690 1 0 |a INTERLEUKIN 10 
690 1 0 |a PLASMID DNA 
690 1 0 |a TRANSFORMING GROWTH FACTOR BETA1 
690 1 0 |a TUMOR NECROSIS FACTOR ALPHA 
690 1 0 |a TUMOR NECROSIS FACTOR ALPHA ANTIBODY 
690 1 0 |a VIRUS VECTOR 
690 1 0 |a CELL TYPE 
690 1 0 |a CLINICAL TRIAL 
690 1 0 |a COMPLEMENT SYSTEM 
690 1 0 |a GENE TARGETING 
690 1 0 |a GENE THERAPY 
690 1 0 |a HUMAN 
690 1 0 |a MAJOR CLINICAL STUDY 
690 1 0 |a MEDIATOR 
690 1 0 |a META ANALYSIS 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a REVIEW 
690 1 0 |a RHEUMATOID ARTHRITIS 
690 1 0 |a ARTHRITIS, RHEUMATOID 
690 1 0 |a GENE THERAPY 
690 1 0 |a GENETIC VECTORS 
690 1 0 |a HUMANS 
700 1 |a Annenkov, A. 
700 1 |a Herman, C. 
700 1 |a Triantaphyllopoulos, K. 
700 1 |a Gould, D. 
700 1 |a Dreja, H. 
700 1 |a Moyes, S.P. 
700 1 |a Croxford, J.L. 
700 1 |a Mageed, R.A. 
700 1 |a Podhajcer, O.L. 
700 1 |a Baker, D. 
773 0 |d 1998  |g v. 12  |h pp. 29-41  |k n. 1  |p Drugs Aging  |x 1170229X  |t Drugs and Aging 
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856 4 0 |u https://doi.org/10.2165/00002512-199812010-00004  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_1170229X_v12_n1_p29_Chernajovsky  |y Handle 
856 4 0 |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_1170229X_v12_n1_p29_Chernajovsky  |y Registro en la Biblioteca Digital 
961 |a paper_1170229X_v12_n1_p29_Chernajovsky  |b paper  |c PE 
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999 |c 63950