Psoriasis is a T-cell-mediated disease that cam be triggered b! l mf&tion with group A P-haemolytic streptococci. It 1s proposed that, bsoriatL skill lesions are initiated by exotoxin-a&uteri T c-ells. and persist because of specific T cells that react both ulith streptococcal M protein and a skin determinant, possibly a llariant of kcr, rtin. As discussed here b15 Helgi Valdimarsson and colleagues, cytokines scleased by the superanti& (SAg)-stimulated T cells could induce or enhance the expression of the crossreactive autoantigen, leading to the rescue and actirution of autoreactive T cells. In this way, the SAgdetermined T-cell receptor V/3 phenotype would be maintained 1~~ T cells in psoriatic lesions.

Psoriasis affects approximately 2% of Caucasians. It is commonly present as persistent plaques on the skin of the knees, elbows or scalp, and a significant proportion of patients may also develop a chronic arthritis. The characteristic skin lesion is persistent, erythematous, indurated and scaly, reflecting infiltration of inflammatory cells and increased proliferation and turnover of keratinocytes. It is this latter feature that distinguishes psoriasis from other inflammatory skin diseases. The infiltrates in the dermis and the deeper layers of the epidermis mostly comprise macrophages and T cells’.‘. Psoriasis tends to be chronic, although spontaneous remissions may occur. Psoriatic skin lesions may also present in a ‘guttate’form-as an acute outhreak of small (1 mm) lesions on the trunk, frequently associated with a preceding history of streptococcal throat infection. Guttate psoriasis tends to be a self-limiting disorder, the lesions clearing after approximately 12 weeks, although 70% of patients develop the chronic plaque form of the disease within a year; eruption of guttate psoriasis is sometimes observed in patients who have already presented with chronic plaques.