Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Chernajovsky, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chernajovsky, Y.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Rheumatology 1999; 38: 804-806
© 1999 British Society for Rheumatology


Editorials

Gene transfer as therapy for rheumatoid arthritis: why, what and how?

Y. Chernajovsky

Kennedy Institute of Rheumatology, 1 Aspenlea Road, Hammersmith, London W6 8LH, UK

Historically, chemically derived drugs have been pursued because of the relative ease of mass production and simple delivery. Chemical modification of drugs in order to increase their effectiveness and lower the side-effects has provided the majority of the drugs in use today. However, synthetic drugs target cellular reactions which are also part of homeostatic/physiological functions, and so they may have non-specific secondary effects in healthy tissues and organs which could be detrimental to patients.

Over the last decade, biomedical research has increased our knowledge regarding the pathological processes and soluble factors involved in the autoimmune and inflammation-mediated destruction of cartilage and bone. The identification of pathogenic factors such as cytokines, matrix metalloproteases, chemokines and angiogenic factors has led to the search for chemical, biological and genetically engineered antagonists. Also, the cells which produce these soluble factors have been targeted in order to inhibit their pathogenic function or induce their death . . . [Full Text of this Article]

Acknowledgments

Notes

References


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?