Abstract
Specific inhibition of the cytokine tumour necrosis factor α (TNFα) has yielded dramatic improvements in the symptoms, signs, and quality of life of patients with chronic inflammatory diseases of Th1 phenotype such as rheumatoid arthritis (RA),1– 9 psoriatic arthritis (PsA),10– 14 ankylosing spondylitis,15– 17 psoriasis,18– 21 and Crohn’s disease.22, 23 The ability of anti-TNFα therapy to inhibit disease progression in RA5, 6, 24 and PsA14, 25 as evidenced by retardation of joint destruction by x ray analysis, has also been documented. Although these clinical results have been clearly demonstrated, our understanding of disease pathophysiology and demonstration of the specific cellular and immunohistochemical effects of new treatments continue to evolve. This review focuses on what has been recently learnt about the mechanism of treatment in PsA and psoriasis.