Mizukawa Yoshiko, Shiohara Tetsuo
Department of Dermatology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan.
Curr Allergy Asthma Rep. 2009 Jan;9(1):71-7. doi: 10.1007/s11882-009-0011-8.
Effector memory T cells are uniquely specialized to mediate protective immunity. However, their excessive activation may result in the development of organ-specific inflammatory diseases, which have not been extensively studied. Fixed drug eruption (FDE), a localized variant of drug-induced dermatoses characterized by relapse in the same location, is a prototypic disorder mediated by excessive activation of effector memory T cells, which are resident in the lesional epidermis. A variety of clinical and pathologic features uniquely observed in FDE lesions can be explained by the presence of CD8(+) intraepidermal T cells with the effector memory phenotype in the FDE lesion. This review focuses on how these T cells are generated, retained in the epidermis, and activated to cause epidermal damage.
效应记忆T细胞具有独特的专门化功能,可介导保护性免疫。然而,它们的过度激活可能导致器官特异性炎症性疾病的发生,而这方面尚未得到广泛研究。固定性药疹(FDE)是药物性皮肤病的一种局限性变体,其特征为在同一部位复发,是由驻留在皮损表皮中的效应记忆T细胞过度激活介导的典型疾病。FDE皮损中独特观察到的各种临床和病理特征可以通过FDE皮损中具有效应记忆表型的CD8(+)表皮内T细胞的存在来解释。本综述重点关注这些T细胞是如何产生、保留在表皮中以及被激活从而导致表皮损伤的。