Valdimarsson H, Baker B S, Jónsdóttir I, Powles A, Fry L
Dept of Immunology, National University Hospital, Reykjavík, Iceland.
Immunol Today. 1995 Mar;16(3):145-9. doi: 10.1016/0167-5699(95)80132-4.
Psoriasis is a T-cell-mediated disease that can be triggered by infection with group A beta-haemolytic streptococci. It is proposed that psoriatic skin lesions are initiated by exotoxin-activated T cells, and persist because of specific T cells that react both with streptococcal M protein and a skin determinant, possibly a variant of keratin. As discussed here by Helgi Valdimarsson and colleagues, cytokines released by the superantigen (SAg)-stimulated T cells could induce or enhance the expression of the crossreactive autoantigen, leading to the rescue and activation of autoreactive T cells. In this way, the SAg-determined T-cell receptor V beta phenotype would be maintained by T cells in psoriatic lesions.
银屑病是一种由T细胞介导的疾病，可由A组β溶血性链球菌感染引发。有人提出，银屑病皮肤病变由外毒素激活的T细胞引发，并因特定T细胞而持续存在，这些T细胞既能与链球菌M蛋白反应，又能与一种皮肤决定簇反应，这种决定簇可能是角蛋白的变体。正如赫尔吉·瓦尔迪马松及其同事在此所讨论的，超抗原（SAg）刺激的T细胞释放的细胞因子可诱导或增强交叉反应性自身抗原的表达，从而导致自身反应性T细胞的挽救和激活。通过这种方式，银屑病皮损中的T细胞将维持由SAg决定的T细胞受体Vβ表型。
