Schwarz T, Urbanska A, Gschnait F, Luger T A
J Immunol. 1987 Mar 1;138(5):1457-63.
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.
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。