Schacter B, Lederman M M, LeVine M J, Ellner J J
J Immunol. 1983 May;130(5):2484-7.
Exposure to ultraviolet radiation (UVR) has been implicated in the predisposition to certain neoplasms and leads to viral reactivation. Natural killer (NK) activity may play a role in immunosurveillance and response to certain viral infections. We have evaluated the sensitivity to UVR of human NK activity, a nonproliferative function, and the proliferative response to the mitogen phytohemagglutinin (PHA). In vitro exposure to UVR resulted in a dose-dependent inhibition of NK activity and response to PHA. The wavelength dependence for UVR inhibition of NK activity and of the PHA response of lymphocytes were virtually superimposable at wavelengths at or above 300 nm, but NK activity was less sensitive to UVR at 260 and 280 nm. Maximal sensitivity for both functions was found at 260 nm, consistent with a nucleic acid chromophore mediating UVR inhibition of both activities. The DNA-directed drugs mitomycin C, acridine orange, and adriamycin at concentrations that inhibit proliferation are poor inhibitors of NK activity. These results suggest that UVR inhibition of NK activity as well as proliferation may be mediated by a nucleic acid chromophore. NK activity, however, is less sensitive to direct damage of DNA by alkylation, distortion, or oxidation. At 300 nm, the amount of radiation required to inhibit NK activity and proliferation is within the range penetrating to the dermis and capillaries during environmental exposure to sunlight.
暴露于紫外线辐射(UVR)与某些肿瘤的易感性有关,并会导致病毒再激活。自然杀伤(NK)活性可能在免疫监视以及对某些病毒感染的反应中发挥作用。我们评估了人类NK活性(一种非增殖功能)对UVR的敏感性以及对丝裂原植物血凝素(PHA)的增殖反应。体外暴露于UVR会导致NK活性和对PHA的反应呈剂量依赖性抑制。在300nm及以上波长时,UVR对NK活性和淋巴细胞PHA反应的抑制作用的波长依赖性几乎是重叠的,但在260和280nm时,NK活性对UVR的敏感性较低。在260nm处发现这两种功能的最大敏感性,这与介导UVR对这两种活性抑制作用的核酸发色团一致。浓度足以抑制增殖的DNA导向药物丝裂霉素C、吖啶橙和阿霉素对NK活性的抑制作用较弱。这些结果表明,UVR对NK活性以及增殖的抑制作用可能由核酸发色团介导。然而,NK活性对DNA因烷基化、扭曲或氧化而受到的直接损伤不太敏感。在300nm时,抑制NK活性和增殖所需的辐射量处于环境暴露于阳光期间穿透到真皮和毛细血管的范围内。