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紫外线照射的表皮细胞会产生一种白细胞介素1活性的特异性抑制剂。

UV-irradiated epidermal cells produce a specific inhibitor of interleukin 1 activity.

作者信息

Schwarz T, Urbanska A, Gschnait F, Luger T A

出版信息

J Immunol. 1987 Mar 1;138(5):1457-63.

PMID:3492552
Abstract

UV irradiation of epidermal cells (EC) in vitro and in vivo leads to an enhanced synthesis of the immunostimulating cytokine interleukin 1 (IL 1). However, UV exposure in vivo also results in local as well as systemic immunosuppression. Therefore, it was tested whether UV-exposed murine EC in culture in addition to IL 1 release an inhibitor of IL 1 activity. Supernatants of UV-irradiated BALB/c EC and of a transformed keratinocyte cell line (Pam 212) were evaluated for their ability to suppress IL 1-mediated thymocyte proliferation. Crude supernatants derived from either UV-exposed or unirradiated EC did not interfere with IL 1 activity. When supernatants were subjected to HPLC gel filtration, fractions eluting at approximately 40 kD significantly blocked the activity of EC-derived IL 1 and murine recombinant IL 1. The release of this inhibitory cytokine (EC-derived contra-IL 1 [EC-contra-IL 1]) was confined to UV-exposed BALB/c or Pam 212 keratinocytes, since no inhibitory activity was detected in supernatants of unirradiated cells. EC-contra-IL 1 also blocked IL 1-induced fibroblast proliferation but did not suppress IL 2 or IL 3 activity. Moreover, EC-contra-IL 1 did not inhibit spontaneous proliferation of a variety of cell lines (Pam 212, P388D1, L 929, EL 4). With the use of chromatofocusing EC-contra-IL 1 exhibited a pI of 8.8, and upon reversed-phase chromatography it eluted within three distinct peaks. Therefore, murine UV-exposed EC, in addition to the production of immunoenhancing cytokines, also may release immunosuppressing mediators and thereby participate in UV-induced immunosuppression. These findings further support the notion that the epidermis may not only be considered as a simple barrier against harmful agents but represents an active element of the immune system.

摘要

体外和体内表皮细胞(EC)经紫外线照射后,免疫刺激细胞因子白细胞介素1(IL - 1)的合成会增强。然而,体内紫外线照射也会导致局部以及全身免疫抑制。因此,研究人员测试了体外培养的经紫外线照射的小鼠表皮细胞除了释放IL - 1外,是否还会释放IL - 1活性抑制剂。对经紫外线照射的BALB/c表皮细胞和转化的角质形成细胞系(Pam 212)的上清液抑制IL - 1介导的胸腺细胞增殖的能力进行了评估。来自经紫外线照射或未照射的表皮细胞的粗制上清液均未干扰IL - 1活性。当对上清液进行高效液相色谱凝胶过滤时,在约40 kD处洗脱的组分显著阻断了表皮细胞来源的IL - 1和小鼠重组IL - 1的活性。这种抑制性细胞因子(表皮细胞来源的抗IL - 1 [EC - 抗IL - 1])的释放仅限于经紫外线照射的BALB/c或Pam 212角质形成细胞,因为在未照射细胞的上清液中未检测到抑制活性。EC - 抗IL - 1也阻断了IL - 1诱导的成纤维细胞增殖,但不抑制IL - 2或IL - 3活性。此外,EC - 抗IL - 1不抑制多种细胞系(Pam 212、P388D1、L 929、EL 4)的自发增殖。通过色谱聚焦法,EC - 抗IL - 1的pH值为8.8,在反相色谱中它在三个不同的峰中洗脱。因此,经紫外线照射的小鼠表皮细胞除了产生免疫增强细胞因子外,还可能释放免疫抑制介质,从而参与紫外线诱导的免疫抑制。这些发现进一步支持了这样一种观点,即表皮不仅可被视为抵御有害物质的简单屏障,而且是免疫系统的一个活跃组成部分。

相似文献

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UV-irradiated epidermal cells produce a specific inhibitor of interleukin 1 activity.紫外线照射的表皮细胞会产生一种白细胞介素1活性的特异性抑制剂。
J Immunol. 1987 Mar 1;138(5):1457-63.
2
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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。
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Epidermal cells synthesize a cytokine with interleukin 3-like properties.表皮细胞合成一种具有白细胞介素3样特性的细胞因子。
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CD11b+ macrophages that infiltrate human epidermis after in vivo ultraviolet exposure potently produce IL-10 and represent the major secretory source of epidermal IL-10 protein.
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Human epidermal cells and squamous carcinoma cells synthesize a cytokine that augments natural killer cell activity.人表皮细胞和鳞状癌细胞合成一种可增强自然杀伤细胞活性的细胞因子。
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A cytokine cascade including prostaglandin E2, IL-4, and IL-10 is responsible for UV-induced systemic immune suppression.包括前列腺素E2、白细胞介素-4和白细胞介素-10在内的细胞因子级联反应是紫外线诱导全身免疫抑制的原因。
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Properties of murine and human epidermal cell-derived thymocyte-activating factor.鼠源和人源表皮细胞衍生的胸腺细胞激活因子的特性
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Proopiomelanocortin-derived peptides are synthesized and released by human keratinocytes.
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Evidence that ultraviolet B radiation induces tolerance and impairs induction of contact hypersensitivity by different mechanisms.有证据表明,紫外线B辐射通过不同机制诱导耐受性并损害接触性超敏反应的诱导。
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