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紫外线B照射和尿刊酸异构体对树突状细胞迁移的影响。

The effect of ultraviolet B irradiation and urocanic acid isomers on dendritic cell migration.

作者信息

Moodycliffe A M, Kimber I, Norval M

机构信息

Department of Medical Microbiology, University of Edinburgh Medical School, U.K.

出版信息

Immunology. 1992 Nov;77(3):394-9.

PMID:1478685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1421727/
Abstract

Irradiation with ultraviolet-B light (UV-B) suppresses some cell-mediated immune responses to a variety of antigens, including contact sensitizers. Following UV irradiation there is modulation of Langerhans' cells' markers and keratinocytes are induced to synthesize and secrete tumour necrosis factor-alpha (TNF-alpha). Cis-urocanic acid (cis-UCA) has been suggested as a photoreceptor for UV and has been demonstrated to suppress immune responses in several experimental systems. UCA is found naturally in the stratum corneum as the trans-isomer and converts to the cis-isomer on irradiation. In the present study the migration of dendritic cells (DC) to lymph nodes following UV-B irradiation or epicutaneous application of UCA isomers was examined in unsensitized mice and mice sensitized with fluorescein isothiocyanate (FITC). It was found that UV-B irradiation alone induced DC migration to draining lymph nodes (DLN) and that UV-B irradiation prior to skin sensitization at the same site enhanced DC migration. A maximum number of DC was present in DLN 48 hr following irradiation. In sensitized mice, the percentage of DC bearing FITC and the quantity of FITC per DC was unaltered by prior UV exposure. In contrast, neither isomer of UCA had any significant effect on DC numbers in sensitized or unsensitized mice. It was concluded that UV-B irradiation induced the migration of DC from the epidermis to draining lymph nodes, an effect possibly mediated by TNF-alpha release, while UCA may act by a different mechanism, perhaps via histamine-like receptors in the epidermis.

摘要

紫外线B光(UV-B)照射可抑制对多种抗原(包括接触性致敏剂)的一些细胞介导的免疫反应。紫外线照射后,朗格汉斯细胞标志物会发生调节,角质形成细胞被诱导合成并分泌肿瘤坏死因子-α(TNF-α)。顺式尿刊酸(cis-UCA)被认为是紫外线的光感受器,并已在多个实验系统中被证明可抑制免疫反应。尿刊酸在角质层中天然以反式异构体形式存在,照射后会转化为顺式异构体。在本研究中,在未致敏小鼠和用异硫氰酸荧光素(FITC)致敏的小鼠中,检测了UV-B照射或经皮应用尿刊酸异构体后树突状细胞(DC)向淋巴结的迁移情况。发现单独的UV-B照射可诱导DC迁移至引流淋巴结(DLN),并且在同一部位进行皮肤致敏之前的UV-B照射可增强DC迁移。照射后48小时,DLN中存在最大数量的DC。在致敏小鼠中,预先暴露于紫外线对携带FITC的DC百分比和每个DC的FITC数量没有影响。相比之下,尿刊酸的两种异构体对致敏或未致敏小鼠的DC数量均无任何显著影响。得出的结论是,UV-B照射诱导DC从表皮迁移至引流淋巴结,这一效应可能由TNF-α释放介导,而尿刊酸可能通过不同机制起作用,也许是通过表皮中的组胺样受体。

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1
The effect of ultraviolet B irradiation and urocanic acid isomers on dendritic cell migration.紫外线B照射和尿刊酸异构体对树突状细胞迁移的影响。
Immunology. 1992 Nov;77(3):394-9.
2
Role of tumour necrosis factor-alpha in ultraviolet B light-induced dendritic cell migration and suppression of contact hypersensitivity.肿瘤坏死因子-α在紫外线B诱导的树突状细胞迁移及接触性超敏反应抑制中的作用
Immunology. 1994 Jan;81(1):79-84.
3
Dermal tumour necrosis factor-alpha induces dendritic cell migration to draining lymph nodes, and possibly provides one stimulus for Langerhans' cell migration.皮肤肿瘤坏死因子-α诱导树突状细胞迁移至引流淋巴结,并且可能为朗格汉斯细胞的迁移提供一种刺激。
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Antigen-presenting activity of draining lymph node cells from mice painted with a contact allergen during ultraviolet carcinogenesis.紫外线致癌过程中接触性变应原涂抹小鼠引流淋巴结细胞的抗原呈递活性
J Immunol. 1991 Mar 15;146(6):1717-21.
5
cis-urocanic acid suppression of contact hypersensitivity induction is mediated via tumor necrosis factor-alpha.顺式尿刊酸对接触性超敏反应诱导的抑制作用是通过肿瘤坏死因子-α介导的。
J Immunol. 1992 May 15;148(10):3072-8.
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Cis-urocanic acid, a product formed by ultraviolet B irradiation of the skin, initiates an antigen presentation defect in splenic dendritic cells in vivo.顺式尿刊酸是皮肤经紫外线B照射后形成的一种产物,它在体内引发脾脏树突状细胞的抗原呈递缺陷。
J Invest Dermatol. 1988 Feb;90(2):92-9. doi: 10.1111/1523-1747.ep12462045.
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Differential effects of a monoclonal antibody to cis-urocanic acid on the suppression of delayed and contact hypersensitivity following ultraviolet irradiation.抗顺式尿刊酸单克隆抗体对紫外线照射后迟发型和接触性超敏反应抑制的不同作用
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Tumour necrosis factor-alpha is required for accumulation of dendritic cells in draining lymph nodes and for optimal contact sensitization.肿瘤坏死因子-α是引流淋巴结中树突状细胞聚集以及最佳接触致敏所必需的。
Immunology. 1995 Jan;84(1):31-5.
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Characterization of a monoclonal antibody to cis-urocanic acid: detection of cis-urocanic acid in the serum of irradiated mice by immunoassay.顺式尿刊酸单克隆抗体的特性:通过免疫测定法检测受辐照小鼠血清中的顺式尿刊酸。
Immunology. 1993 Aug;79(4):667-72.
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A monoclonal antibody to cis-urocanic acid prevents the ultraviolet-induced changes in Langerhans cells and delayed hypersensitivity responses in mice, although not preventing dendritic cell accumulation in lymph nodes draining the site of irradiation and contact hypersensitivity responses.一种针对顺式尿刊酸的单克隆抗体可防止紫外线诱导的小鼠朗格汉斯细胞变化和迟发型超敏反应,尽管不能阻止照射部位引流淋巴结中的树突状细胞积聚和接触性超敏反应。
J Invest Dermatol. 1995 Aug;105(2):264-8. doi: 10.1111/1523-1747.ep12318410.

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本文引用的文献

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Dendritic cells and T cells transfer sensitization for delayed-type hypersensitivity after skin painting with contact sensitizer.在用接触致敏剂进行皮肤涂抹后,树突状细胞和T细胞会传递迟发型超敏反应的致敏作用。
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Mechanism of systemic immune suppression by UV irradiation in vivo. II. The UV effects on number and morphology of epidermal Langerhans cells and the UV-induced suppression of contact hypersensitivity have different wavelength dependencies.紫外线体内照射引起全身免疫抑制的机制。II. 紫外线对表皮朗格汉斯细胞数量和形态的影响以及紫外线诱导的接触性超敏反应抑制具有不同的波长依赖性。
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The role of dendritic cells in the initiation of immune responses to contact sensitizers. I. In vivo exposure to antigen.树突状细胞在接触性致敏剂免疫反应启动中的作用。I. 体内抗原暴露。
Cell Immunol. 1985 Sep;94(2):427-34. doi: 10.1016/0008-8749(85)90266-7.
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Keratinocyte derived T-cell growth factor (KTGF) is identical to granulocyte macrophage colony stimulating factor (GM-CSF).角质形成细胞衍生的T细胞生长因子(KTGF)与粒细胞巨噬细胞集落刺激因子(GM-CSF)相同。
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Granulocyte/macrophage colony-stimulating factor and interleukin 1 mediate the maturation of murine epidermal Langerhans cells into potent immunostimulatory dendritic cells.粒细胞/巨噬细胞集落刺激因子和白细胞介素1介导小鼠表皮朗格汉斯细胞成熟为强效免疫刺激性树突状细胞。
J Exp Med. 1988 Feb 1;167(2):700-5. doi: 10.1084/jem.167.2.700.
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Localization of antigen on lymph node dendritic cells after exposure to the contact sensitizer fluorescein isothiocyanate. Functional and morphological studies.接触致敏剂异硫氰酸荧光素暴露后抗原在淋巴结树突状细胞上的定位。功能和形态学研究。
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