Rheumatology 1999; 38: 804-806
© 1999 British Society for Rheumatology
Editorials |
Gene transfer as therapy for rheumatoid arthritis: why, what and how?
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
Acknowledgments
Notes
References