Dittmar H C, Weiss J M, Termeer C C, Denfeld R W, Wanner M B, Skov L, Barker J N, Schöpf E, Baadsgaard O, Simon J C
Department of Dermatology, University of Freiburg, Germany.
J Invest Dermatol. 1999 Mar;112(3):322-5. doi: 10.1046/j.1523-1747.1999.00527.x.
Ultraviolet B (UVB, 290-320 nm) radiation is known to suppress the immune function of epidermal Langerhans cells. We have recently described that in vitro UVB irradiation perturbs the antigen-presenting cell function of Langerhans cells by inhibiting their expression of functional B7 costimulatory molecules (B7-1, B7-2). The aim of this study was to determine wavelength-specific UV effects on Langerhans cells function in vivo, specifically UVB and UVA-1. To address this issue, volunteers were irradiated on the sun protected volar aspects of their forearms with 3 x minimal erythema dose of UVB (Philips TL-12) and UVA-1 (UVASUN 5000 Mutzhaas). Langerhans cells were isolated from suction blister roofs immediately following irradiation. Langerhans cells isolated from UVB- but not from UVA-1-irradiated skin failed to activate naïve resting allogeneic T cells (mixed epidermal cell leukocyte reaction) or primed tetanus toxoid reactive autologous T cells. Langerhans cells isolated from sham-irradiated or UVA-1-irradiated skin strongly upregulated B7-2 molecules during short-term tissue culture. By contrast, Langerhans cells from UVB-irradiated skin did not upregulate B7-2 molecules. Furthermore, exogenous stimulation of the B7 pathway by anti-CD28 stimulatory monoclonal antibodies restored the capacity of UVB-irradiated Langerhans cells to activate both alloreactive and tetanus toxoid-reactive T cells, implying suppressed antigen-presenting cell activities and perturbed B7 expression of Langerhans cells isolated from UVB-irradiated skin are related. Those studies demonstrate that in vivo UVB, but not UVA-1, interferes with the activation-dependent upregulation of B7 molecules on Langerhans cells, which in turn is of functional relevance for the perturbed antigen-presenting cell function of Langerhans cells within UVB- but not UVA-1-irradiated skin.
已知紫外线B（UVB，290 - 320纳米）辐射会抑制表皮朗格汉斯细胞的免疫功能。我们最近描述了体外UVB照射通过抑制功能性B7共刺激分子（B7 - 1、B7 - 2）的表达来扰乱朗格汉斯细胞的抗原呈递细胞功能。本研究的目的是确定紫外线对体内朗格汉斯细胞功能的波长特异性影响，特别是UVB和UVA - 1。为了解决这个问题，用3倍最小红斑量的UVB（飞利浦TL - 12）和UVA - 1（UVASUN 5000 Mutzhaas）照射志愿者前臂受阳光保护的掌侧。照射后立即从负压水疱顶部分离朗格汉斯细胞。从UVB照射而非UVA - 1照射皮肤分离的朗格汉斯细胞无法激活未致敏的静息同种异体T细胞（混合表皮细胞白细胞反应）或已致敏的破伤风类毒素反应性自体T细胞。从假照射或UVA - 1照射皮肤分离的朗格汉斯细胞在短期组织培养期间强烈上调B7 - 2分子。相比之下，来自UVB照射皮肤的朗格汉斯细胞未上调B7 - 2分子。此外，抗CD28刺激单克隆抗体对B7途径的外源性刺激恢复了UVB照射的朗格汉斯细胞激活同种异体反应性和破伤风类毒素反应性T细胞的能力，这意味着从UVB照射皮肤分离的朗格汉斯细胞的抗原呈递细胞活性受抑制和B7表达受扰乱是相关的。这些研究表明，体内UVB而非UVA - 1会干扰朗格汉斯细胞上B7分子的激活依赖性上调，这反过来又与UVB照射而非UVA - 1照射皮肤内朗格汉斯细胞的抗原呈递细胞功能受扰乱具有功能相关性。
