紫外线辐射对免疫功能的影响。
Ultraviolet radiation effects on immunologic function.
作者信息
Granstein R D
机构信息
Wellman Laboratories of Photomedicine, Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston 02114.
出版信息
Reg Immunol. 1990 Mar-Apr;3(2):112-9.
Studies over the past two decades have established that exposure to ultraviolet radiation (UVR) has profound effects on immunity. Most of this work was done in animal models with limited data from human studies. Exposure to UVR inhibits the induction of contact hypersensitivity in mice systemically at high doses and locally at low doses, associated with the appearance of transferable T suppressor cells. In some strains of mice, chronic UVR exposure results in the occurrence of highly immunogenic cutaneous malignancies which are rejected upon transplantation to syngeneic recipients. However, within the primary host the tumor is protected from destruction, at least in part, by the appearance of T suppressor cells. Syngeneic animals exposed to large doses of UVR also permit the growth of these transplanted tumors and this phenomenon also results, at least in part, from the presence of suppressor cells. Interestingly, these suppressor cells appear to recognize UVR-induced regressor tumors as a class within a given mouse strain, suggesting that they recognize shared determinants. The mechanisms of these examples of UVR-induced immunosuppression are not completely clear, but perhaps relate to changes in Langerhans cell function and/or epidermal cell release of cytokines induced by UVR. Exposure to UVR in vitro alters the ability of epidermal cells and Langerhans cells to present some antigens. Keratinocytes alter their secretion of specific cytokines after exposure to UVR and are induced to produce immunosuppressive factors. Immunosuppressed patients also have increased rates of skin cancer, suggesting immunologic involvement in regulation of cutaneous oncogenesis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
过去二十年的研究表明,紫外线辐射(UVR)暴露对免疫有深远影响。这项工作大多是在动物模型中完成的,来自人体研究的数据有限。高剂量全身性和低剂量局部性的UVR暴露均会抑制小鼠接触性超敏反应的诱导,这与可转移的T抑制细胞的出现有关。在某些小鼠品系中,长期UVR暴露会导致高免疫原性皮肤恶性肿瘤的发生,这些肿瘤移植到同基因受体后会被排斥。然而,在原发宿主体内,肿瘤至少部分地受到T抑制细胞出现的保护而免遭破坏。暴露于大剂量UVR的同基因动物也允许这些移植肿瘤生长,这种现象至少部分也是由抑制细胞的存在导致的。有趣的是,在给定的小鼠品系中,这些抑制细胞似乎将UVR诱导的消退性肿瘤识别为一类,这表明它们识别共同的决定簇。UVR诱导免疫抑制的这些例子的机制尚不完全清楚,但可能与朗格汉斯细胞功能的变化和/或UVR诱导的表皮细胞细胞因子释放有关。体外UVR暴露会改变表皮细胞和朗格汉斯细胞呈递某些抗原的能力。角质形成细胞在暴露于UVR后会改变其特定细胞因子的分泌,并被诱导产生免疫抑制因子。免疫抑制患者的皮肤癌发病率也有所增加,这表明免疫在人类皮肤肿瘤发生的调控中发挥作用。(摘要截短于250字)