Morison W L, Pike R A, Kripke M L
Photodermatol. 1985 Aug;2(4):195-204.
Exposure of mice to UVB (280-320 nm) radiation is known to suppress the development of contact hypersensitivity (CHS) to chemicals that are applied subsequently to unirradiated skin, and this suppression is associated with the generation of suppressor lymphocytes. In this study, the systemic effect of other wavebands of nonionizing radiation on the development of CHS has been tested. Large doses of visible (greater than 400 nm) radiation produced a small but consistent systemic suppression of CHS in mice. In contrast, a large dose of UVA (320-400 nm) radiation did not suppress CHS but, rather, enhanced this immune response. Exposure of both mice and guinea pigs to sunlight produced systemic suppression of CHS. The suppression could be transferred to normal syngeneic animals by injection of splenic lymphoid cells obtained from animals that exhibited suppression, indicating that suppressor cells are associated with sunlight-induced systemic suppression of CHS. The immunomodulatory effect of sunlight was partially abrogated by a Mylar filter or prior application of a sunscreen containing para-aminobenzoic acid to the exposed skin. Thus, wavelengths mainly in the UVB portion of sunlight (295-320 nm) are responsible for sunlight-induced suppression of CHS, although wavelengths in the visible region may also play a role.
已知将小鼠暴露于UVB（280 - 320纳米）辐射会抑制随后应用于未照射皮肤的化学物质的接触性超敏反应（CHS）的发展，并且这种抑制与抑制性淋巴细胞的产生有关。在本研究中，测试了其他非电离辐射波段对CHS发展的全身效应。大剂量的可见光（大于400纳米）辐射对小鼠的CHS产生了微小但持续的全身抑制。相比之下，大剂量的UVA（320 - 400纳米）辐射并未抑制CHS，反而增强了这种免疫反应。将小鼠和豚鼠暴露于阳光下会产生CHS的全身抑制。这种抑制可以通过注射从表现出抑制作用的动物获得的脾脏淋巴细胞转移到正常的同基因动物，这表明抑制细胞与阳光诱导的CHS全身抑制有关。阳光的免疫调节作用被聚酯薄膜滤光片或事先在暴露皮肤涂抹含对氨基苯甲酸的防晒霜部分消除。因此，阳光中主要在UVB部分（295 - 320纳米）的波长是阳光诱导的CHS抑制的原因，尽管可见光区域的波长也可能起作用。
