Journal
ARTHRITIS RESEARCH
Volume 4, Issue 4, Pages 266-273Publisher
BMC
DOI: 10.1186/ar419
Keywords
adenosine receptor; inflammation; methotrexate; rheumatoid arthritis
Categories
Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000096] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR041911] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM056268] Funding Source: NIH RePORTER
- NCRR NIH HHS [M01 RR000096, M01RR00096] Funding Source: Medline
- NIAMS NIH HHS [R01 AR041911, AR41911] Funding Source: Medline
- NIGMS NIH HHS [GM56268, R01 GM056268] Funding Source: Medline
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Despite the recent introduction of biological response modifiers and potent new small-molecule antirheumatic drugs, the efficacy of methotrexate is nearly unsurpassed in the treatment of inflammatory arthritis. Although methotrexate was first introduced as an antiproliferative agent that inhibits the synthesis of purines and pyrimidines for the therapy of malignancies, it is now clear that many of the anti-inflammatory effects of methotrexate are mediated by adenosine. This nucleoside, acting at one or more of its receptors, is a potent endogenous anti-inflammatory mediator. In confirmation of this mechanism of action, recent studies in both animals and patients suggest that adenosine-receptor antagonists, among which is caffeine, reverse or prevent the anti-inflammatory effects of methotrexate.
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