Rheumatology Advance Access originally published online on June 8, 2004
Rheumatology 2004 43(8):946-948; doi:10.1093/rheumatology/keh234
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Rheumatology Vol. 43 No. 8 © British Society for Rheumatology 2004; all rights reserved
Editorial |
Tacrolimus therapy in rheumatoid arthritis
Centre for Rheumatic Diseases, Glasgow Royal Infirmary, 84 Castle Street, Glasgow G4 0SF, UK
Correspondence to: R. Madhok. E-mail: gcl103@clinmed.gla.ac.uk
| The first 150 words of the full text of this article appear below. |
Our understanding of the pathogenesis of rheumatoid arthritis (RA) has recently improved significantly and this has been paralleled by the availability of highly effective agents directed against TNF-
as well as the more effective use of existing agents, often in combination. However, a sizeable proportion of patients are unresponsive to these therapeutic approaches. Furthermore the long-term consequences of continued TNF- blockade are not known. It is therefore critically important for us to continue to develop new therapeutic strategies that target the broad range of cell types that we consider to be important in the initiation and perpetuation of inflammatory synovitis. Rather than focusing narrowly on the targeting of specific effector molecules such as TNF-, there is a strong case to be made for improving our capability further upstream in the inflammatory cascade, for example in T-cell inhibition.
For some time now it has been clear that the T cell