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Specific targeting of activated T cells to treat severe psoriasis vulgaris and generalized pustular psoriasis was first done by using intravenous anti-CD4 monoclonal antibodies.^1-2 Improvement occurred; however, a rapid flare was also noted. Recently, systemic treatment with an interleukin 2–diphtheria fusion toxin (DAB₃₈₉IL-2) was shown to be effective in about 40% of patients with severe psoriasis.³

Basiliximab is a specific chimeric monoclonal antibody against the -chain of the IL-2 receptor (CD25). The drug is registered for the prevention of graft rejection together with conventional immunosuppressive therapies.^4-5 Because of its long terminal half-life of 7 days and good tolerability, basiliximab may be assumed to be beneficial in dermatoses where activated T cells are thought to mediate the disease.

Two patients with severe, recalcitrant psoriasis vulgaris were treated with basiliximab after providing informed consent. Psoriasis involvement was monitored weekly using the psoriasis area and severity index (PASI). Expression of CD25 on . . . [Full Text of this Article]

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