IRF-2 haploinsufficiency causes enhanced imiquimod-induced psoriasis-like skin inflammation

Psoriasis is a T-cell-mediated immunologic skin disease with a complex pathogenesis where both genetic and environmental factors are involved [1–4]. Although the mechanism of psoriasis has not been fully understood, it has been reported that psoriasis can be induced or exacerbated by IFN-α treatment [5–10]. More direct evidence for the involvement of type I IFN in development of psoriasis comes from studies on interferon regulatory factor (IRF)-2 knockout mice. IRF-2 protein binds the same regulatory sequences as IRF-1, which suppresses transcription of IFN-inducible genes [11].