Proksch E, Brasch J, Sterry W
Department of Dermatology, University of Kiel, Germany.
Br J Dermatol. 1996 Apr;134(4):630-8.
Previous studies have shown that barrier requirements regulate epidermal liquid and DNA synthesis. In the present study, we examined the possibility that the integrity of the permeability barrier influences epidermal Langerhans cells involved with the immune response. Barrier disruption was achieved by treatment of human skin with acetone, sodium dodecylsulphate (SDS), or tape stripping, until a 10-20-fold increase in transepidermal water loss was achieved. Serial biopsies were performed 6-168 h after treatment, and Langerhans cells were complexed with anti-CD1a (Leu6) or S-100 antibodies, and visualized with an immunoperoxidase technique. Acetone treatment resulted in an increase in epidermal Langerhans cell density, reaching a maximum of 94% over control (P < 0.01) by 24 and 48 h post-treatment. Following SDS treatment or tape stripping, epidermal Langerhans cell density was increased by 100 and 175% (P < 0.01), respectively. There was a linear correlation between the degree of barrier disruption and the increase in epidermal Langerhans cell density. Studies with the Ki-S3 proliferation-associated nuclear antigen revealed a two- to threefold increase in epidermal proliferation after barrier disruption. The time curves of the increase in Langerhans cell density and the increase in epidermal proliferation were similar, suggesting that there was a coordinate regulation. In contrast with our previous studies employing patch test reactions to allergens or irritants, disruption of barrier function neither resulted in an increased dermal Langerhans cell density, nor influenced T lymphocytes (CD3+, Leu4+), macrophages (KiM8+), ICAM-1 or ELAM-1 expression in the skin. In addition, barrier disruption did not result in either dermal inflammation or epidermal spongiosis. In summary, these findings support our hypothesis that the permeability barrier influences epidermal Langerhans cell density, which is involved in maintaining an immunological barrier.
以往研究表明，屏障需求可调节表皮液体和DNA合成。在本研究中，我们探讨了通透性屏障的完整性影响参与免疫反应的表皮朗格汉斯细胞的可能性。通过用丙酮、十二烷基硫酸钠（SDS）处理人皮肤或胶带剥离来破坏屏障，直至经表皮水分流失增加10 - 20倍。处理后6 - 168小时进行连续活检，将朗格汉斯细胞与抗CD1a（Leu6）或S - 100抗体复合，并用免疫过氧化物酶技术进行可视化。丙酮处理导致表皮朗格汉斯细胞密度增加，处理后24小时和48小时比对照最高增加94%（P < 0.01）。SDS处理或胶带剥离后，表皮朗格汉斯细胞密度分别增加100%和175%（P < 0.01）。屏障破坏程度与表皮朗格汉斯细胞密度增加之间存在线性相关性。对Ki - S3增殖相关核抗原的研究表明，屏障破坏后表皮增殖增加两到三倍。朗格汉斯细胞密度增加和表皮增殖增加的时间曲线相似，表明存在协同调节。与我们之前使用针对变应原或刺激物的斑贴试验反应的研究不同，屏障功能破坏既未导致真皮朗格汉斯细胞密度增加，也未影响皮肤中T淋巴细胞（CD3 +，Leu4 +）、巨噬细胞（KiM8 +）、细胞间黏附分子-1（ICAM - 1）或内皮白细胞黏附分子-1（ELAM - 1）的表达。此外，屏障破坏未导致真皮炎症或表皮海绵形成。总之，这些发现支持了我们的假设，即通透性屏障影响表皮朗格汉斯细胞密度，而表皮朗格汉斯细胞密度参与维持免疫屏障。
