Heng M C, Kloss S G, Kuehn C S, Chase D G
Br J Dermatol. 1985 May;112(5):517-32. doi: 10.1111/j.1365-2133.1985.tb15259.x.
The sequence of events leading to the formation of a psoriatic plaque induced by tape-stripping was studied using light and electron microscopy. Among the earliest changes noted were increased mobility of the epidermal Langerhans cells across the basement membrane, evidence of Langerhans cell-lymphocyte interaction, and increased Langerhans cells 'activity' or 'cytotoxicity'. These changes were seen as early as 2 min after stripping and remained until the development of clinical psoriasis. Collections of epidermal lymphocytes showing the features of blastoid transformation while in contact with processes from activated Langerhans cells, suggest the involvement of Ia antigens in this process. We postulate that these findings are a manifestation of an increased immune responsiveness to trauma, controlled by genes located at the HLA-D locus of the major histocompatibility complex, and mediated by enhanced cellular interactions. The appearance of basal keratinocyte herniations (BKH) at 1-3 weeks after stripping, coincided with the development of clinical psoriasis. Neutrophils made their appearance at the same time as, or slightly before, the appearance of BKH, and are suspected to play a role in the development of these structures. We believe that BKH maintain epidermal proliferation through the persistence of the epidermal-stromal interaction.
运用光学显微镜和电子显微镜,研究了胶带剥离诱导银屑病斑块形成过程中的一系列事件。最早观察到的变化包括表皮朗格汉斯细胞穿过基底膜的迁移增加、朗格汉斯细胞与淋巴细胞相互作用的证据,以及朗格汉斯细胞“活性”或“细胞毒性”增强。这些变化在剥离后2分钟就可见到,并一直持续到临床银屑病出现。表皮淋巴细胞聚集,在与活化的朗格汉斯细胞的突起接触时呈现母细胞样转化特征,提示Ia抗原参与了这一过程。我们推测,这些发现是对创伤免疫反应增强的一种表现,受位于主要组织相容性复合体HLA - D位点的基因控制,并由增强的细胞间相互作用介导。剥离后1 - 3周出现的基底角质形成细胞疝(BKH),与临床银屑病的发展同时出现。中性粒细胞在BKH出现的同时或稍早出现,推测其在这些结构的发展中起作用。我们认为,BKH通过表皮 - 基质相互作用的持续存在来维持表皮增殖。