Lappin M B, Kimber I, Dearman R J, Norval M
Department of Medical Microbiology, University of Edinburgh Medical School, Scotland, UK.
Exp Dermatol. 1996 Oct;5(5):286-94. doi: 10.1111/j.1600-0625.1996.tb00131.x.
Following the application of sensitizing chemicals to the skin, hapten-bearing Langerhans cells (LC) and possibly other cutaneous dendritic cells (DC) migrate to the draining lymph nodes (DLN) of mice and induce the proliferation of antigen specific effector T cells. This migration of DC to the DLN is required for the induction of primary immune responses. In certain strains of mice, irradiation with ultraviolet-B light (UVB) before sensitization results in the suppression of contact hypersensitivity responses. In vitro investigations have suggested that one influence of UVB is to modify the ability of Langerhans cells (LC) to present antigen. In the present investigation, putative UVB-induced alterations in lymph node DC in vivo were examined. Lymph node DC were analysed following exposure of C3H/HeN mice to an immunosuppressive dose of UVB (1440 J/m2) 48 and 24 h prior to skin painting with the sensitizers fluorescein isothiocyanate or oxazolone. In functional studies, DC prepared from the DLN of contact sensitized mice were examined for their ability to induce hapten-specific secondary T-lymphocyte proliferative responses or mixed lymphocyte reactions in vitro. In neither case was the activity of DC influenced by local exposure to an immunosuppressive dose of UVB. The migration of LC from the epidermis to the draining lymph node in response to contact sensitization is associated with increased expression of several membrane determinants necessary for effective antigen presentation, including intercellular adhesion molecule-1 (ICAM-1; CD54), B7-2 (CD86) and Ia antigen. The expression of these molecules was identical on DC isolated from the DLN of UVB-irradiated and from control, unirradiated mice. Thus, the immunosuppressive effect of UVB on the cutaneous immune system may not necessarily reflect changes in the antigen-presenting DC that accumulate in the DLN following skin sensitization.
在将致敏化学物质应用于皮肤后，携带半抗原的朗格汉斯细胞（LC）以及可能的其他皮肤树突状细胞（DC）迁移至小鼠的引流淋巴结（DLN），并诱导抗原特异性效应T细胞增殖。DC向DLN的这种迁移是诱导初次免疫反应所必需的。在某些品系的小鼠中，致敏前用紫外线B（UVB）照射会导致接触性超敏反应受到抑制。体外研究表明，UVB的一个作用是改变朗格汉斯细胞（LC）呈递抗原的能力。在本研究中，检测了体内UVB诱导的淋巴结DC的假定改变。在用异硫氰酸荧光素或恶唑酮致敏剂进行皮肤涂抹前48小时和24小时，将C3H/HeN小鼠暴露于免疫抑制剂量的UVB（1440 J/m²）后，对淋巴结DC进行分析。在功能研究中，检测了从接触致敏小鼠的DLN制备的DC在体外诱导半抗原特异性二次T淋巴细胞增殖反应或混合淋巴细胞反应的能力。在这两种情况下，DC的活性均未受到局部暴露于免疫抑制剂量UVB的影响。LC从表皮迁移至引流淋巴结以响应接触致敏，这与有效抗原呈递所需的几种膜决定簇的表达增加有关，包括细胞间黏附分子-1（ICAM-1；CD54）、B7-2（CD86）和Ia抗原。从UVB照射小鼠和未照射的对照小鼠的DLN分离的DC上，这些分子的表达是相同的。因此，UVB对皮肤免疫系统的免疫抑制作用不一定反映皮肤致敏后在DLN中积聚的抗原呈递DC的变化。
