Antagonism of co-stimulatory molecules has provided a new dimension for treatment of the autoimmune diseases.[5] To have a proof of the concept that psoriasis SCID mouse model can be used to evaluate therapeutic efficacy of pharmacologic agents targeting the T-cell co-stimulatory system, we designed a double-blinded, placebo controlled study using the SCID-psoriasis xenografts.[5] The transplanted psoriatic plaques on the SCID mice (n = 12) were treated with CTLA4IgG (10 mg/kg/week), a natural inhibitor of CD28/B7 co-stimulatory signals. Here, CD28 is linked to psoriasis.