Relationship between ultraviolet radiation-induced immunosuppression and carcinogenesis.
Relationship between ultraviolet radiation-induced immunosuppression and carcinogenesis.
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紫外线辐射诱导的免疫抑制与致癌的关系。
DOI：
10.1111/1523-1747.ep12399400
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Golomb,C
中科院分区：
文献类型：
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作者：
Streilein,JW;Taylor,JR;Vincek,V;Kurimoto,I;Richardson,J;Tie,C;Medema,JP;Golomb,C
紫外线B（UVB）辐射损害皮肤免疫系统的能力已被广泛记录，有充分的理由相信，UVB引起的损害是一个关键的，虽然允许，在阳光引起的皮肤癌的发展因素。证据的总结表明，急性，低剂量的UVB协议，这类似于定量和定性的方式，人类通常经历的阳光照射，改变皮肤免疫系统在至少两个重要的方式：他们削弱了皮肤抗原的接触超敏反应的诱导，并诱导抗原特异性耐受。在小鼠中，有令人信服的证据表明，免疫遗传因素决定UVB辐射是否会损害接触性超敏反应的诱导。含有相关多态性等位基因的遗传位点包括肿瘤坏死因子-α和脂多糖。由于UVB辐射对接触性超敏反应诱导的影响可以通过皮内注射亚炎症剂量的肿瘤坏死因子-α或顺式尿刊酸来模拟，因此解释UVB辐射对UVB敏感个体作用机制的有利假设是，表皮中反式至顺式尿刊酸的UVB依赖性转化触发了过量肿瘤坏死因子-α的皮内释放。通过将朗格汉斯细胞和其他局部抗原呈递细胞暂时固定在皮肤内，不能满足将半抗原带到引流淋巴结至敏感的幼稚半抗原特异性T细胞的要求，并且接触性超敏反应不能发展。由于UVB敏感性和UVB抗性特征也已在人类中得到证实，因此提出了这样的假设，即这些特征类似地受免疫遗传因素的控制，并且一系列免疫敏感性基因有助于发展日光诱导的皮肤癌的风险。
The capacity of ultraviolet B (UVB) radiation to damage the cutaneous immune system has been extensively documented, and there is good reason to believe that UVB-induced damage is a critical, albeit permissive, factor in the development of sunlight-induced skin cancers. A summary of the evidence shows that acute, low-dose UVB protocols, which resemble quantitatively and qualitatively the manner in which human beings typically experience sun exposure, alter the cutaneous immune system in at least two important ways: they impair the induction of contact hypersensitivity to cutaneous antigens, and induce antigen-specific tolerance. In mice there is compelling evidence that immunogenetic factors dictate whether UVB radiation will impair contact hypersensitivity induction or not. The genetic loci that contain the relevant polymorphic alleles include tumor necrosis factor-α and lipopolysaccharide. Because the effects of UVB radiation on contact hypersensitivity induction are mimicked by intracutaneous injections of subinflammatory doses of tumor necrosis factor-α or cis-urocanic acid, the favored hypothesis to explain the mechanism of action of UVB radiation in UVB-susceptible individuals is that UVB-dependent transformation of trans-to cis-urocanic acid in the epidermis triggers the intracutaneous release of excess amounts of tumor necrosis factor-α. By transiently immobilizing Langerhans cells and other local antigen-presenting cells within the skin, the requirement that hapten be brought to the draining lymph node to sensitive naive hapten-specific T cells is not met, and contact hypersensitivity fails to develop. Because the UVB-susceptibility and UVB-resistance traits have also been demonstrated in human beings, the hypothesis is advanced that these traits are similarly under control of immunogenetic factors, and that a constellation of immune susceptibility genes contributes to the risk of developing sunlight-induced skin cancer.