High levels of the pro-inflammatory cytokine tumour necrosis factor (TNF) have been associated with many diseases including rheumatoid arthritis (RA), ankylosing spondylitis (AS), inflammatory bowel disease (IBD) and psoriasis. Although it has been clear for twenty-five years that TNF plays a major role in RA and AS, two major questions remain unanswered: (1) What mechanism underlies the loss of control of TNF levels in patients? (2) How does TNF exert its detrimental effects? Nonetheless, biological anti-TNF drugs have become the most successful treatment of these conditions with a third of patients entering remission, and the global market for biological TNF inhibitors is now estimated at around US$35 billions. However, their use is limited by their cost, the fact that they need to be injected, non-negligible side effects and the development of resistance due to the protein (thus antigenic) nature of these TNF inhibitors. It looks inevitable that new approaches to lower the amount of TNF should be considered. To do this, a better understanding of the regulation of TNF expression is necessary.
Keywords: 3′ untranslated region; Arthritis; Gene expression; Heart valve disease; Tumour necrosis factor.
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