The complex pathogenesis of immune-mediated inflammatory diseases (IMIDs) has 
been extensively investigated and dysregulation of cytokines, such as tumour 
necrosis factor (TNF) has been shown to play a dominant role in the pathogenesis 
of various IMIDs, such as rheumatoid arthritis, ankylosing spondylitis, Crohn's 
disease, ulcerative colitis, psoriasis and psoriatic arthritis. The subsequent 
development of biological agents capable of blocking TNF has led to important 
advances in the pharmacotherapy of such diseases and confirmed the concept of a 
common pathophysiology among IMIDs with TNF having a predominant role. Five TNF 
inhibitors have currently been approved for treatment of one or more IMIDs; 
these include infliximab, etanercept, adalimumab, golimumab and certolizumab 
pegol. Given the similarities in the pathogenic background of IMIDs, one could 
expect that anti-TNF agents be similarly effective and with comparable 
tolerability profiles; however, this may not be the case. Structural and 
pharmacological differences among the anti-TNF drugs are likely to result in 
differences in efficacy and tolerability among the agents in the different 
IMIDs, together with differences in potency, therapeutic dose ranges, dosing 
regimens, administration routes, and propensity for immunogenicity. Among the 
five TNF inhibitors approved for treatment of IMIDs, adalimumab has the widest 
range of indications. Data from controlled clinical trials of adalimumab, 
showing its excellent efficacy and tolerability in a wide range of indications, 
are supported by real-world long-term data from observational studies, which 
confirm the value of adalimumab as a suitable choice in the management of IMIDs.