Morison W L, Kelley S P
J Natl Cancer Inst. 1985 Feb;74(2):525-7.
Repeated exposure of female C3H/HeNCR- mice to sunlight prevented the normal immunologic rejection of a UV-induced tumor. This systemic immunologic alteration was transferred to syngeneic lethally X-irradiated animals with lymphoid cells from mice exposed to sunlight. The lymphoid cells also were able to suppress the capacity of lymphoid cells from normal animals to reject a UV-induced tumor. The 295- to 320-nm wave band appeared to be responsible for this immunosuppressive effect of sunlight because suppression was prevented by filtration of the radiation through Mylar and by application of a sunscreen containing para-aminobenzoic acid. These observations may have importance in understanding the pathogenesis of sunlight-induced skin cancer in humans.
将雌性C3H/HeNCR-小鼠反复暴露于阳光下,可阻止紫外线诱导肿瘤的正常免疫排斥反应。这种全身性免疫改变可通过将暴露于阳光下的小鼠的淋巴细胞转移至同基因致死性X射线照射的动物身上而实现。这些淋巴细胞还能够抑制正常动物的淋巴细胞排斥紫外线诱导肿瘤的能力。295至320纳米波段似乎是造成阳光这种免疫抑制作用的原因,因为通过聚酯薄膜过滤辐射以及涂抹含对氨基苯甲酸的防晒霜可防止这种抑制作用。这些观察结果对于理解人类阳光诱导皮肤癌的发病机制可能具有重要意义。