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紫外线照射的表皮细胞释放的因子所致的免疫抑制:暴露于UVA或UVB辐射后对接触性超敏反应和迟发型超敏反应产生的选择性影响

Immunosuppression by factors released from UV-irradiated epidermal cells: selective effects on the generation of contact and delayed hypersensitivity after exposure to UVA or UVB radiation.

作者信息

Kim T Y, Kripke M L, Ullrich S E

机构信息

Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

J Invest Dermatol. 1990 Jan;94(1):26-32. doi: 10.1111/1523-1747.ep12873322.

DOI:10.1111/1523-1747.ep12873322
PMID:2295834
Abstract

Exposure of murine epidermal cells to UV radiation in vitro causes the release of immunoregulatory factors that mimic some of the immunosuppressive effects of in vivo UV irradiation. The purpose of this study was to investigate the spectrum of immune responses affected following i.v. injection of supernatants obtained from cultures of epidermal cells exposed in vitro to UV radiation. Treatment of primary epidermal cell cultures or transformed keratinocytes (Pam 212 cells) with UVB (280-320 nm) radiation caused the release of factors that suppressed the induction of delayed hypersensitivity to alloantigen and trinitrophenyl-modified self-antigens in syngeneic and allogeneic mice. Contrary to expectations, however, the injection of supernatants from UVB-irradiated epidermal cells had no effect on the induction of contact hypersensitivity to trinitrochlorobenzene. On the other hand, treatment of the keratinocytes with UVA radiation (320-400 nm, filtered to remove wavelengths in the UVB region) resulted in the release of a factor that suppressed contact but not delayed hypersensitivity. Neither the UVA-induced nor the UVB-induced suppressive factor inhibited the generation of an antibody response to sheep erythrocytes, indicating that, like the suppression that occurs after in vivo exposure to UV radiation, the suppression induced by factors from UV-irradiated keratinocytes is selective in nature. These data support the hypothesis that soluble keratinocyte-derived suppressive factors are involved in the induction of systemic immune suppression by UV radiation. In addition, they suggest that multiple suppressive factors, having different immunosuppressive properties, are produced by different wavelengths of UV radiation.

摘要

体外将小鼠表皮细胞暴露于紫外线辐射会导致免疫调节因子的释放,这些因子可模拟体内紫外线照射的一些免疫抑制作用。本研究的目的是调查静脉注射从体外暴露于紫外线辐射的表皮细胞培养物中获得的上清液后所影响的免疫反应谱。用UVB(280 - 320nm)辐射处理原代表皮细胞培养物或转化的角质形成细胞(Pam 212细胞)会导致因子释放,这些因子会抑制同基因和异基因小鼠对同种异体抗原和三硝基苯基修饰的自身抗原的迟发型超敏反应的诱导。然而,与预期相反,注射来自UVB照射的表皮细胞的上清液对三硝基氯苯接触性超敏反应的诱导没有影响。另一方面,用UVA辐射(320 - 400nm,过滤以去除UVB区域的波长)处理角质形成细胞会导致一种因子的释放,该因子抑制接触性超敏反应但不抑制迟发型超敏反应。UVA诱导的和UVB诱导的抑制因子均不抑制对绵羊红细胞的抗体反应的产生,这表明,与体内暴露于紫外线辐射后发生的抑制一样,紫外线照射的角质形成细胞产生的因子所诱导的抑制在本质上是选择性的。这些数据支持可溶性角质形成细胞衍生的抑制因子参与紫外线辐射诱导的全身免疫抑制的假说。此外,它们表明不同波长的紫外线辐射会产生具有不同免疫抑制特性的多种抑制因子。

相似文献

1
Immunosuppression by factors released from UV-irradiated epidermal cells: selective effects on the generation of contact and delayed hypersensitivity after exposure to UVA or UVB radiation.紫外线照射的表皮细胞释放的因子所致的免疫抑制:暴露于UVA或UVB辐射后对接触性超敏反应和迟发型超敏反应产生的选择性影响
J Invest Dermatol. 1990 Jan;94(1):26-32. doi: 10.1111/1523-1747.ep12873322.
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Systemic suppression of delayed-type hypersensitivity by supernatants from UV-irradiated keratinocytes. An essential role for keratinocyte-derived IL-10.紫外线照射的角质形成细胞上清液对迟发型超敏反应的全身抑制作用。角质形成细胞衍生的白细胞介素-10的重要作用。
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Supernatants from UVB radiation-exposed keratinocytes inhibit Langerhans cell presentation of tumor-associated antigens via IL-10 content.紫外线B辐射暴露的角质形成细胞的上清液通过白细胞介素-10含量抑制朗格汉斯细胞对肿瘤相关抗原的呈递。
J Leukoc Biol. 1995 Aug;58(2):234-40. doi: 10.1002/jlb.58.2.234.
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Suppression of the immune response to alloantigen by factors released from ultraviolet-irradiated keratinocytes.紫外线照射的角质形成细胞释放的因子对同种异体抗原免疫反应的抑制作用。
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Activation of keratinocytes with psoralen plus UVA radiation induces the release of soluble factors that suppress delayed and contact hypersensitivity.
J Invest Dermatol. 1991 Dec;97(6):995-1000. doi: 10.1111/1523-1747.ep12491903.
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Inhibition of the induction of contact hypersensitivity by a UV-mediated epidermal cytokine.
J Invest Dermatol. 1986 Aug;87(2):289-91. doi: 10.1111/1523-1747.ep12696708.
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Aloe barbadensis extracts reduce the production of interleukin-10 after exposure to ultraviolet radiation.
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UVB and UVC, but not UVA, potently induce the appearance of T6- DR+ antigen-presenting cells in human epidermis.紫外线B(UVB)和紫外线C(UVC),而非紫外线A(UVA),能有效诱导人表皮中T6-DR +抗原呈递细胞的出现。
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Local effects of UV radiation on immunization with contact sensitizers. I. Down-regulation of contact hypersensitivity by application of TNCB to UV-irradiated skin.紫外线辐射对接触致敏剂免疫的局部影响。I. 将三硝基氯苯应用于紫外线照射的皮肤对接触性超敏反应的下调作用。
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Increased expression of Fas on human epidermal cells after in vivo exposure to single-dose ultraviolet (UV) B or long-wave UVA radiation.在体内暴露于单剂量紫外线(UV)B或长波紫外线A辐射后,人表皮细胞上Fas表达增加。
Br J Dermatol. 2002 Dec;147(6):1199-206. doi: 10.1046/j.1365-2133.2002.04787.x.

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The immune-modulating cytokine and endogenous Alarmin interleukin-33 is upregulated in skin exposed to inflammatory UVB radiation.
在暴露于炎症性 UVB 辐射的皮肤中,免疫调节细胞因子和内源性警报素白细胞介素-33 上调。
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Effects of acute, low-dose UVB radiation on the induction of contact hypersensitivity to diphenylcyclopropenone in man.急性低剂量中波紫外线辐射对人体二苯环丙烯酮接触性超敏反应诱导的影响。
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