Ultraviolet B radiation suppresses endocytosis, subsequent maturation, and migration activity of Langerhans cell-like dendritic cells
Ultraviolet B radiation suppresses endocytosis, subsequent maturation, and migration activity of Langerhans cell-like dendritic cells
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DOI：
10.1046/j.0022-202x.2004.22206.x
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发表时间：
2004-02-01
影响因子：
6.5
通讯作者：
Horio, T
中科院分区：
文献类型：
--
作者：
Mizuno, K;Okamoto, H;Horio, T
朗格汉斯细胞通过液相胞饮和受体介导的内吞作用捕获外源性抗原，并迁移到淋巴结，在那里它们将加工的抗原呈递给T细胞。紫外线B辐射损害朗格汉斯细胞的抗原呈递功能，导致接触性超敏反应的抗原特异性免疫抑制。我们测试的概念，紫外线B辐射抑制朗格汉斯细胞的内吞活性，导致受损的迁移和成熟。人单核细胞来源的朗格汉斯细胞样树突状细胞，采取了荧光黄或异硫氰酸荧光素葡聚糖专门迁移响应6Ckine/次级淋巴趋化因子，并成熟，证明了在异基因混合淋巴细胞反应中的CD 54和CD 86表达和有效的刺激活性的增加。将朗格汉斯细胞样树突状细胞暴露于20-40 mJ/cm 2的紫外线B辐射，可降低其在液相胞饮（通过摄取荧光黄测量）和受体介导的胞吞（通过摄取异硫氰酸荧光素葡聚糖测量）中的内吞活性。紫外线B辐射还抑制了膜皱褶和CD 32表达。紫外线照射的，内吞朗格汉斯细胞样树突状细胞有较少的运动向6Ckine，表达较少的CD 54和CD 86，并有较低的有效刺激活性，在同种异体混合淋巴细胞反应比非照射，内吞朗格汉斯细胞样树突状细胞。内吞作用上调肿瘤坏死因子α生产的朗格汉斯细胞样树突状细胞，但以前的紫外线B辐射抑制这种增强。这些数据表明，受损的内吞作用和随后的抑制迁移和成熟的朗格汉斯细胞的紫外线B辐射可能有助于局部免疫抑制的接触性超敏反应。
Langerhans cells capture exogenous antigens through fluid phase pinocytosis and receptor-mediated endocytosis and migrate to lymph nodes, where they present processed antigen to T cells. Ultraviolet B radiation impairs the antigen-presenting function of Langerhans cells, resulting in antigen-specific immunosuppression of contact hypersensitivity. We tested the notion that ultraviolet B radiation inhibits the endocytic activity of Langerhans cells, leading to impaired migration and maturation. Human monocyte-derived Langerhans cell-like dendritic cells that took up lucifer yellow or fluorescein isothiocyanate dextran exclusively migrated in response to 6Ckine/secondary lymphoid chemokine, and matured, as evidenced by an increase in CD54 and CD86 expression and potent stimulatory activity in allogeneic mixed lymphocyte reaction. Exposing Langerhans cell-like dendritic cells to 20-40 mJ per cm(2) of ultraviolet B radiation reduced their endocytic activity in fluid phase pinocytosis (measured by uptake of lucifer yellow) and in receptor-mediated endocytosis (measured by uptake of fluorescein isothiocyanate dextran). Membrane ruffling and CD32 expression were also suppressed by ultraviolet B radiation. Ultraviolet B-irradiated, endocytosing Langerhans cell-like dendritic cells had less movement towards 6Ckine, expressed less CD54 and CD86, and had less effective stimulatory activity in allogeneic mixed lymphocyte reaction than nonirradiated, endocytosing Langerhans cell-like dendritic cells. Endocytosis upregulated tumor necrosis factor alpha production by Langerhans cell-like dendritic cells, but prior ultraviolet B radiation inhibited this enhancement. These data suggested that impaired endocytosis and subsequent inhibitory migration and maturation of Langerhans cells by ultraviolet B radiation could contribute to local immunosuppression of contact hypersensitivity.