van Praag M C, Out-Luyting C, Claas F H, Vermeer B J, Mommaas A M
Department of Dermatology, University Hospital Leiden, The Netherlands.
J Invest Dermatol. 1991 Oct;97(4):629-33. doi: 10.1111/1523-1747.ep12483065.
Exposure of mice or humans to solar or artificial ultraviolet radiation (UV) has been shown to induce a number of changes in the immune system that may influence their susceptibility to skin tumors. The protective effect of sunscreens on these changes is not clear. Thirty-two patients with a variety of dermatoses routinely undergoing treatment with standard UVB (n = 19) or PUVA (n = 13) therapy were studied. One of the two tested sunscreens or its vehicle was applied to the right flexor forearm immediately prior to each total-body UV exposure. Epidermal sheets were obtained by the suction-blister method from the left flexor forearm before treatment and from both flexor forearms after 4 weeks of photo- or photochemotherapy and used as stimulator epidermal cells (EC) in the mixed epidermal cell-lymphocyte reaction (MECLR). After 4 weeks of either UVB or PUVA therapy the MECLR responses on EC from both arms were markedly decreased. Neither the tested sunscreens nor their vehicles prevented the UV-induced suppression of the alloactivating capacity. The failure of sunscreens to protect against the UV-induced suppression of the alloactivating capacity could be explained in two ways. First, the energy not absorbed by the sunscreen could be sufficient to induce suppression of the alloactivating capacity. An alternative explanation could be systemic immune suppression by UV. In order to discriminate between these possibilities only the right forearms of 10 healthy volunteers, treated with a sunscreen or its vehicle, were irradiated with UVB during 4 weeks. In this manner systemic immune suppression by UVB could be excluded. This experiment resulted in a similar suppression of the MECLR responses, as induced by total body UVB irradiation, without any protection by the sunscreen. Apparently, the UV dose not absorbed by the sunscreen was capable to induce suppression of the alloactivating capacity. Our results indicate that people protected from sunburn by sunscreens may be exposed to UV for a long period of time, and thereby subject themselves to its immunosuppressive action.
已表明,小鼠或人类暴露于太阳或人工紫外线辐射(UV)会在免疫系统中引发许多变化,这些变化可能会影响他们对皮肤肿瘤的易感性。防晒霜对这些变化的保护作用尚不清楚。对32例患有各种皮肤病且常规接受标准UVB(n = 19)或PUVA(n = 13)治疗的患者进行了研究。在每次全身UV照射前,将两种测试防晒霜之一或其赋形剂立即涂抹于右屈侧前臂。通过吸疱法在治疗前从左屈侧前臂获取表皮片,并在光疗或光化学疗法4周后从两侧屈侧前臂获取表皮片,用作混合表皮细胞 - 淋巴细胞反应(MECLR)中的刺激表皮细胞(EC)。UVB或PUVA治疗4周后,双臂EC的MECLR反应均明显降低。测试的防晒霜及其赋形剂均未阻止UV诱导的同种异体激活能力的抑制。防晒霜未能预防UV诱导的同种异体激活能力抑制可通过两种方式解释。首先,未被防晒霜吸收的能量可能足以诱导同种异体激活能力的抑制。另一种解释可能是UV引起的全身免疫抑制。为了区分这些可能性,仅对10名健康志愿者的右前臂涂抹防晒霜或其赋形剂,并在4周内用UVB照射。通过这种方式,可以排除UVB引起的全身免疫抑制。该实验导致了与全身UVB照射诱导的MECLR反应类似的抑制,且没有防晒霜的任何保护作用。显然,未被防晒霜吸收的UV剂量能够诱导同种异体激活能力的抑制。我们的结果表明,使用防晒霜防止晒伤的人可能长时间暴露于UV,从而使其自身受到其免疫抑制作用。