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紫外线B辐射优先诱导正常人皮肤中记忆性CD4 + T细胞的募集:单次暴露后的长期效应。

UVB radiation preferentially induces recruitment of memory CD4+ T cells in normal human skin: long-term effect after a single exposure.

作者信息

Di Nuzzo S, Sylva-Steenland R M, de Rie M A, Das P K, Bos J D, Teunissen M B

机构信息

Department of Dermatology, Academic Medical Center, University of Amsterdam, The Netherlands.

出版信息

J Invest Dermatol. 1998 Jun;110(6):978-81. doi: 10.1046/j.1523-1747.1998.00220.x.

DOI:10.1046/j.1523-1747.1998.00220.x
PMID:9620309
Abstract

Acute, low-doses of ultraviolet (UV)-B radiation affect the immune competent cells of the skin immune system. In this study, we examined the time-dependent changes of the cutaneous T cell population in normal human volunteers following a single local exposure to UV. Solar-simulated UV radiation caused an initial decrease in intraepidermal T cell numbers, even leading to T cell depletion at day 4, whereupon a considerable infiltration of T cells in the epidermis occurred that peaked at day 14. In the dermis the number of T cells was markedly increased at days 2 (peak) and 4 after irradiation, and subsequently declined to the nonirradiated control values at day 10. Double-staining with several T cell markers showed that the T cells, infiltrating the (epi)dermis upon UV exposure, were almost exclusively CD4+ CD45RO+ T cells, expressing an alpha/beta type T cell receptor, but lacking the activation markers HLA-DR, VLA-1, and IL-2R. Application of UVB radiation resulted in similar dynamics of T cells, indicating that the UVB wavelengths within the solar-simulated UV radiation were responsible for the selective influx of CD4+ T cells. In conjunction with UVB-induced alterations in the type and function of antigen-presenting cells (i.e., Langerhans cells and macrophages), the changes of the cutaneous T cell population may also contribute to UVB-induced immunosuppression at skin level in man.

摘要

急性低剂量紫外线B辐射会影响皮肤免疫系统的免疫活性细胞。在本研究中,我们检测了正常人类志愿者单次局部暴露于紫外线后皮肤T细胞群体随时间的变化。模拟太阳光的紫外线辐射导致表皮内T细胞数量最初减少,甚至在第4天导致T细胞耗竭,随后表皮中出现大量T细胞浸润,并在第14天达到峰值。在真皮中,照射后第2天(峰值)和第4天T细胞数量显著增加,随后在第10天降至未照射对照值。用几种T细胞标志物进行双重染色显示,紫外线暴露后浸润(表)皮的T细胞几乎全是CD4+CD45RO+T细胞,表达α/β型T细胞受体,但缺乏活化标志物HLA-DR、VLA-1和IL-2R。紫外线B辐射的应用导致T细胞出现类似的动态变化,表明模拟太阳光的紫外线辐射中的紫外线B波长是CD4+T细胞选择性流入的原因。结合紫外线B诱导的抗原呈递细胞(即朗格汉斯细胞和巨噬细胞)类型和功能的改变,皮肤T细胞群体的变化也可能导致人类皮肤水平上紫外线B诱导的免疫抑制。

相似文献

1
UVB radiation preferentially induces recruitment of memory CD4+ T cells in normal human skin: long-term effect after a single exposure.紫外线B辐射优先诱导正常人皮肤中记忆性CD4 + T细胞的募集:单次暴露后的长期效应。
J Invest Dermatol. 1998 Jun;110(6):978-81. doi: 10.1046/j.1523-1747.1998.00220.x.
2
Solar-simulated ultraviolet irradiation induces selective influx of CD4+ T lymphocytes in normal human skin.模拟太阳紫外线照射可诱导正常人皮肤中CD4+ T淋巴细胞选择性流入。
Photochem Photobiol. 1996 Dec;64(6):988-93. doi: 10.1111/j.1751-1097.1996.tb01866.x.
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Density and proportions of the epidermal T cell population in human sun-exposed skin differ from those in sun-protected skin: preliminary immunohistochemical study.人类暴露于阳光下皮肤与防晒皮肤中表皮T细胞群体的密度和比例不同:初步免疫组织化学研究。
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MHC class II-KO mice are resistant to the immunosuppressive effects of UV light.MHC II类基因敲除小鼠对紫外线的免疫抑制作用具有抗性。
Eur J Dermatol. 2002 Jan-Feb;12(1):10-9.
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Human epidermal cells from ultraviolet light-exposed skin preferentially activate autoreactive CD4+2H4+ suppressor-inducer lymphocytes and CD8+ suppressor/cytotoxic lymphocytes.来自紫外线照射皮肤的人表皮细胞优先激活自身反应性CD4 + 2H4 +抑制诱导淋巴细胞和CD8 +抑制/细胞毒性淋巴细胞。
J Immunol. 1988 Mar 15;140(6):1738-44.
6
Depletion of CD4+ cells exacerbates the cutaneous response to acute and chronic UVB exposure.CD4+细胞的耗竭会加剧皮肤对急性和慢性紫外线B照射的反应。
J Invest Dermatol. 2007 Jun;127(6):1507-15. doi: 10.1038/sj.jid.5700746. Epub 2007 Mar 15.
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In vivo ultraviolet-exposed human epidermal cells activate T suppressor cell pathways that involve CD4+CD45RA+ suppressor-inducer T cells.体内紫外线照射的人表皮细胞激活涉及CD4 + CD45RA +抑制诱导性T细胞的T抑制细胞途径。
J Immunol. 1990 Nov 1;145(9):2854-61.
8
Despite the presence of UVB-induced DNA damage, HLA-DR+ cells from ex vivo UVB-exposed human skin are able to migrate and show no impaired allostimulatory capacity.尽管存在紫外线B(UVB)诱导的DNA损伤,但来自体外UVB照射的人皮肤的HLA-DR+细胞仍能够迁移,并且没有显示出异基因刺激能力受损。
J Invest Dermatol. 1997 Nov;109(5):626-31. doi: 10.1111/1523-1747.ep12337609.
9
Suppressor T cell-activating macrophages in ultraviolet-irradiated human skin induce a novel, TGF-beta-dependent form of T cell activation characterized by deficient IL-2r alpha expression.紫外线照射的人类皮肤中抑制性T细胞激活巨噬细胞可诱导一种新型的、依赖转化生长因子β的T细胞激活形式,其特征为白细胞介素-2受体α表达缺陷。
J Immunol. 1995 Dec 15;155(12):5601-7.
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Rapid recovery of Langerhans cell alloreactivity, without induction of autoreactivity, after in vivo ultraviolet A, but not ultraviolet B exposure of human skin.人体皮肤经体内紫外线A而非紫外线B照射后,朗格汉斯细胞同种异体反应性迅速恢复,且未诱导自身反应性。
J Immunol. 1989 Jun 15;142(12):4213-8.

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