Webber L J, Whang E, De Fabo E C
Department of Dermatology, George Washington University Medical Center, Washington, DC, USA.
Photochem Photobiol. 1997 Oct;66(4):484-92. doi: 10.1111/j.1751-1097.1997.tb03177.x.
Ultraviolet B radiation (280-320 nm) can systemically suppress contact hypersensitivity (CHS), delayed type hypersensitivity (DTH) and tumor rejection responses in mice. Several models have been postulated for the initiation of this UVB-induced immune suppression and, although the complete mechanism is unclear, our early studies suggested that initiation is via the activation of a photoreceptor in the skin, identified as urocanic acid (UCA). Recent preliminary data from our laboratory and others indicated that UVA (320-400 nm)-emitting broad-band sunlamps can also isomerize UCA but may not lead to immune suppression, in contrast to UVB-emitting sunlamps, which cause both effects. Although the reason for this inconsistency is unknown, the emission spectra of UVA lamps contain differing amounts of UVB, UVA-I (340-400 nm) and UVA-II (320-340 nm) from those of UVB sources. In this study we determined a detailed dose-response for the isomerization of UCA in mouse skin using the UVA-I, UVA-II and UVA-I+II wavelength ranges. The dose-response curves obtained were put on an equal energy basis by quantum correction and the possibility of wavelength interaction for this effect investigated. A simple additive wavelength interaction between UVA-I, UVA-II, and UVA-I+II was observed for trans-UCA photoisomerization. This result indicates that the failure of UVA-I, UVA-II or UVA-I+II radiation to induce immune suppression of the CHS response in an animal model is not due to complex wavelength interactions and/or the presence of an in vivo endogenous photosensitizer of UCA isomerization. Other factors, such as downstream blocking by UVA of the cis-UCA generated signal, may be involved.
紫外线B辐射（280 - 320纳米）可全身性抑制小鼠的接触性超敏反应（CHS）、迟发型超敏反应（DTH）和肿瘤排斥反应。关于这种紫外线B诱导的免疫抑制的起始，已经提出了几种模型，尽管完整机制尚不清楚，但我们早期的研究表明，起始是通过皮肤中一种光感受器的激活，这种光感受器被确定为尿刊酸（UCA）。我们实验室和其他实验室最近的初步数据表明，发射UVA（320 - 400纳米）的宽带太阳灯也能使UCA异构化，但与发射紫外线B的太阳灯不同，后者会导致两种效应，而发射UVA的太阳灯可能不会导致免疫抑制。尽管这种不一致的原因尚不清楚，但UVA灯的发射光谱与紫外线B源的发射光谱相比，所含的UVB、UVA-I（340 - 400纳米）和UVA-II（320 - 340纳米）的量不同。在本研究中，我们使用UVA-I、UVA-II和UVA-I + II波长范围确定了小鼠皮肤中UCA异构化的详细剂量反应。通过量子校正将获得的剂量反应曲线置于等能量基础上，并研究了这种效应的波长相互作用可能性。观察到反式UCA光异构化过程中UVA-I、UVA-II和UVA-I + II之间存在简单的加性波长相互作用。这一结果表明，在动物模型中，UVA-I、UVA-II或UVA-I + II辐射未能诱导对CHS反应的免疫抑制，并非由于复杂的波长相互作用和/或存在UCA异构化的体内内源性光敏剂。可能涉及其他因素，例如UVA对顺式UCA产生的信号的下游阻断。
