Psoriasis is a complex inflammatory skin disease in which local vascular changes, T-cell activation, abnormal keratinocyte proliferation and differentiation, and neutrophil activation all contribute to the ongoing disease process. Because of recent interest in T-cell activation as a trigger for psoriatic lesions, we hypothesized that psoriasis may be triggered by superantigens, e.g., toxins of microbial origin that stimulate T cells expressing particular T-cell receptor (TCR) fJ chain variable

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... V fJ) gene segments. Lesional skin biopsies and peripheral blood from two patients with acute exacerbations of their psoriasis that appeared to be triggered by infection were analyzed for TCR VfJ gene expression using monoclonal P revious investigations into the pathogenesis of psoriasis have identified a number of important factors: keratinocyte (HK) proliferation, vascular alterations, dermal influences on HK growth, lymphocyte activation, neutrophil attraction, and activation of dermal macrophages (Me). It remains controversial whether a primary epidermal defect causes elaboration of cytokines that results in increased vascular activation and the infiltration of activated T cells, or whether epidermal hyperproliferation occurs secondary to inductive effects mediated by cytokines derived from infiltrating cells. Careful histologic examination of early lesions, however, has demonstrated that activation of T lymphocytes, endothelial cells, and Me precedes epidermal proliferation [1] . Furthermore, immunosuppressive drugs such as anti-CD3, methotrexate, corticosteroids, UV irradiation, and cyclosporine A are effective in treating psoriasis [2] . Numerous other observations support the concept that an ongoing cellular immune response may contribute to the formation and persistence of psoriatic plaques. Localized collections ofHLA-DR +