Abstract
Both clinical as well as experimental data support the concept of psoriasis being a T-cell-mediated immune disease possibly triggered by bacterial superantigens. Further analysis of its pathogenesis was facilitated by the generation of a xenogeneic transplantation model in which skin from psoriatic patients is grafted onto SCID mice lacking functional B and T cells. Applying this model it was demonstrated that psoriasis can be triggered by bacterial superantigens; this process depends on the presence of immunocytes. Mutated variants of the respective superantigens exhibiting no measurable affinity to HLA class II molecules can function as competitive inhibitors in vivo.
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