Nakamura T, Kurimoto I, Itami S, Yoshikawa K, Streilein J W
Department of Dermatology, Osaka University Medical School, 2-2, Yamadaoka, Suita, 565-0871, Osaka, Japan.
J Dermatol Sci. 2000 Mar;23 Suppl 1:S13-6. doi: 10.1016/s0923-1811(99)00072-9.
Acute low-dose treatment of murine skin with ultraviolet B (UVB) light impairs induction of contact hypersensitivity (CH) to dinitrofluorobenzene (DNFB) in certain inbred strains of mice (termed UVB-susceptible), but not in others (termed UVB-resistant). These deleterious effects of ultraviolet radiation (UVR) are mediated in part by TNF-alpha, which is released from UVR-exposed epidermal and dermal cells. To test the hypothesis that polymorphism of TNF-alpha governs the phenotype of UVB-susceptibility in vivo, various strains of mice received UVB radiation followed by hapten application to induce contact hypersensitivity. Results suggest that the polymorphism at the Tnf-alpha locus dictates UVB susceptibility in vivo.
用紫外线B（UVB）对小鼠皮肤进行急性低剂量处理，会损害某些近交系小鼠（称为UVB敏感型）对二硝基氟苯（DNFB）的接触性超敏反应（CH）诱导，但对其他小鼠（称为UVB抗性型）则无此影响。紫外线辐射（UVR）的这些有害作用部分由TNF-α介导，TNF-α由暴露于UVR的表皮和真皮细胞释放。为了检验TNF-α多态性决定体内UVB易感性表型这一假设，对各种品系的小鼠进行UVB辐射，然后施加半抗原以诱导接触性超敏反应。结果表明，Tnf-α基因座的多态性决定了体内UVB易感性。
