The understanding of the pathogenesis of psoriasis vulgaris has advanced significantly since the therapeutic efficacy of immunosuppressive drugs has drawn attention to the role of immune mechanisms in psoriasis manifestation. Today, the results of many experimental studies provide evidence that psoriasis is largely a T-cell mediated disorder. It may result from antigen-specific activation of T cells in the skin of genetically predisposed individuals. These T cells apparently have a particular functional differentiation and promote the psoriatic skin changes by secreting a certain set of cytokines. Based on the fact that streptococcal throat infections are a trigger of guttate psoriasis, the putative psoriatic antigens are assumed to be in keratinocyte proteins that share structural homologies with streptococcal proteins and thus induce cross-reactive responses of antibacterial T cells against skin components. Together with the particular phenotype of psoriatic skin lesions these findings suggest that psoriasis represents a sterile antibacterial tissue reaction, which is mediated by streptococci-specific T cells that cross-react against epidermal autoantigens.