Psoriasis is a chronic, genetically determined, immune-mediated, inflammatory 
skin disease affecting approximately 2% to 3% of Caucasian population. Given the 
well-established role of the immuno-mediated inflammation in the pathogenesis of 
psoriasis, in the past few years several key steps in the pathogenesis of this 
disease have been elucidated and the increased knowledge led to the development 
of specific drugs, commonly defined as "biologics" targeting one or more of 
these steps. At present an anti-CD11a antibody (efalizumab), an anti-LFA3/CD2 
receptor (alefacept) and 3 antitumor necrosis factor alpha agents (adalimumab, 
etanercept, infliximab) are now commercially available for the treatment of both 
psoriasis and psoriatic arthritis. Recent studies have demonstrated that 
interleukins (IL) 12 and 23 play an important role in the pathophysiology of 
psoriasis. In fact members of the IL-12 family of cytokines have the potential 
to act as the next major cytokine(s) in pathogenesis and the treatment of 
psoriasis. Ustekinumab (CNTO 1275, Centocor Inc, Malvern, PA, USA) is a human 
monoclonal antibody that binds to the shared p40 protein subunit of human 
interleukins 12 and 23 with high affinity and specificity, thereby preventing 
interaction with their surface IL-12Rβ1 receptor. Different clinical studies 
have been conducted to date. In particular a phase II study and two phase III 
studies, PHOENIX 1 together with PHOENIX 2, show very encouraging results. This 
review reports on the latest progress made in the clinical use of biologic drugs 
for psoriasis focusing on the new human IL-12/23 monoclonal antibody, 
ustekinumab, for psoriasis.