Baadsgaard O, Wulf H C, Wantzin G L, Cooper K D
J Invest Dermatol. 1987 Jul;89(1):113-8. doi: 10.1111/1523-1747.ep12580461.
Non-Langerhans cell, antigen-presenting T6- DR+ epidermal cells (EC) appear 3 days following broad band ultraviolet radiation exposure of human skin and are responsible for the increased antigen presentation capacity of EC seen 3 days after UV exposure. To determine the UV wavelengths that induce T6- DR+ EC, volar forearm skin of 10 human volunteers was irradiated in vivo with 4 minimal erythema doses (MED) each of pure UVA (mean 482 J cm-2), UVB (mean 0.390 J cm-2), and UVC (mean 0.397 J cm-2). The purity of the light sources was as follows: UVB, 98% of the emission was in the UVB range; UVC, 97% of the irradiance was in the UVC range; UVA, 100% of the energy had wavelengths longer than 340 nm. Three days after UV irradiation with 4 MED of each wavelength band, suction blister-derived EC suspensions were prepared from the UV-exposed and unirradiated sites. Percentages of T6+ DR+ Langerhans cells (LC) and T6- DR+ EC were quantitated. Relative to control EC, which contained 2.4 +/- 0.3% T6+ DR+ LC, the mean percentage (+/- SEM) of T6+ DR+ LC contained within UV-exposed EC was significantly decreased as follows: UVB, 0.5 +/- 0.2%; UVC, 0.9 +/- 0.1%; UVA, 0.5 +/- 0.2% (n = 10). T6- DR+ EC, absent in control EC, were induced both by UVB, 5.2 +/- 1.7% and UVC; 1.5 +/- 0.4%. Despite the use of more than 1200 times greater doses in J cm-2 of UVA than UVB and UVC, UVA was a poor inducer of T6- DR+ EC (0.5 +/- 0.2%) and in about half of these individuals, T6- DR+ EC were undetectable. The UV wavelengths for induction of T6- DR+ EC lies predominantly within the UVB band, but also to a lesser extent within the UVC band. These wavelengths appear to be analogous to both the wavelengths for generation of increased host susceptibility to UV-induced murine tumors and to the wavelengths for UV-induced systemic suppression of contact hypersensitivity. However, our data indicate that UV wavelengths for decreasing the number of T6+ DR+ LC in humans differs from the wavelengths for induction of systemic suppression of contact hypersensitivity in mice. Taken together, these data suggest that the appearance of T6- DR+ EC, but not the disappearance of T6+ DR+ LC, following UV exposure may be related to the induction of such antigen-specific suppressor T cells.
非朗格汉斯细胞、抗原呈递性T6 - DR +表皮细胞(EC)在人体皮肤接受宽带紫外线照射3天后出现,并且是紫外线照射3天后EC抗原呈递能力增强的原因。为了确定诱导T6 - DR + EC的紫外线波长,对10名人类志愿者的掌侧前臂皮肤进行体内照射,每个波长分别给予4个最小红斑量(MED)的纯UVA(平均482 J/cm²)、UVB(平均0.390 J/cm²)和UVC(平均0.397 J/cm²)。光源的纯度如下:UVB,98%的发射光在UVB范围内;UVC,97%的辐照度在UVC范围内;UVA,100%的能量波长大于340 nm。在每个波长带用4个MED进行紫外线照射3天后,从紫外线照射部位和未照射部位制备抽吸水疱来源的EC悬液。对T6 + DR +朗格汉斯细胞(LC)和T6 - DR + EC的百分比进行定量。相对于对照EC(含有2.4±0.3%的T6 + DR + LC),紫外线照射后EC中T6 + DR + LC的平均百分比(±SEM)显著降低,如下所示:UVB,0.5±0.2%;UVC,0.9±0.1%;UVA,0.5±0.2%(n = 10)。对照EC中不存在的T6 - DR + EC,在UVB照射后诱导产生的比例为5.2±1.7%,UVC照射后为1.5±0.4%。尽管UVA的剂量在J/cm²上比UVB和UVC大1200多倍,但UVA诱导T6 - DR + EC的能力较差(0.5±0.2%),并且在大约一半的个体中,无法检测到T6 - DR + EC。诱导T6 - DR + EC的紫外线波长主要在UVB波段内,但在UVC波段内的程度较小。这些波长似乎既类似于增加宿主对紫外线诱导的小鼠肿瘤易感性的波长,也类似于紫外线诱导的接触性超敏反应全身抑制的波长。然而,我们的数据表明,人类中降低T6 + DR + LC数量的紫外线波长与小鼠中诱导接触性超敏反应全身抑制的波长不同。综上所述,这些数据表明,紫外线照射后T6 - DR + EC的出现,而不是T6 + DR + LC的消失,可能与这种抗原特异性抑制性T细胞的诱导有关。