Shiohara Tetsuo, Mizukawa Yoshiko
Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka, Tokyo, Japan.
Eur J Dermatol. 2007 May-Jun;17(3):201-8. doi: 10.1684/ejd.2007.0149. Epub 2007 May 4.
It is difficult to dissect disease-causing T cells and anti-inflammatory T cells in a biopsy specimen obtained at a given time, which would represent a single time point in the development of the lesions. In fixed drug eruption (FDE), the resting lesions long after clinical resolution have many clues to identify the disease-causing T cells, because they contain a large homogeneous population of CD8(+) T cells that are distributed along the epidermal basal layer and have the capacity to rapidly produce large amounts of IFN-gamma. These intraepidermal CD8(+) T cells are likely to be a major actor in epidermal injury observed in FDE lesions. In this review, we ask how they arise and how they cause epidermal injuries, which present with a wide spectrum of clinical manifestations and are often mistaken as signs of other skin disease.
在给定时间获取的活检标本中,很难区分致病T细胞和抗炎T细胞,因为该标本代表病变发展过程中的单个时间点。在固定性药疹(FDE)中,临床消退很久后的静止性皮损有许多线索可用于识别致病T细胞,因为它们含有大量均匀分布的CD8(+) T细胞,这些细胞沿表皮基底层分布,并且有能力快速产生大量的γ干扰素。这些表皮内CD8(+) T细胞很可能是FDE皮损中观察到的表皮损伤的主要作用因素。在这篇综述中,我们探讨它们是如何产生的以及如何导致表皮损伤,FDE的临床表现多种多样,常被误诊为其他皮肤病的症状。