There is much evidence to support the concept that psoriasis is a type 1 autoimmune disease, primarily mediated by interferon gamma and other inflammatory cytokines. There has been renewed interest in the role of components of the innate immune system, however,and it may be that overlap between the innate and acquired arms of the immune system can better explain immunopathogenesis in psoriasis. Relevant cell types, receptors, and immune mediators within these traditional boundaries of the immune system are discussed.Finally, pathogenic contributions from important psoriatic mouse models and recent genomic data using the new gene chip technology are elaborated.