Greene M I, Sy M S, Kripke M, Benacerraf B
Proc Natl Acad Sci U S A. 1979 Dec;76(12):6591-5. doi: 10.1073/pnas.76.12.6591.
UV light irradiation of BALB/c mice was found to result in impairment of antigen-presenting cell function. Adherent trinitrophenyl-derivatized cells from the peritoneal exudate cell population or the spleen of UV-treated donors could not induce hapten-specific delayed hypersensitivity responses in UV-irradiated syngeneic mice, whereas adherent trinitrophenyl-derivatized cells from normal mice were able to do so. The failure to induce immunity in UV-treated mice by utilizing UV-treated adherent antigen-presenting cells was associated with the development of antigen-specific suppressor T cells. The implication of these results for UV-induced carcinogenesis is discussed.
研究发现,对BALB/c小鼠进行紫外线照射会导致抗原呈递细胞功能受损。来自紫外线处理供体的腹膜渗出细胞群体或脾脏中贴壁的三硝基苯基衍生细胞,无法在紫外线照射的同基因小鼠中诱导半抗原特异性迟发型超敏反应,而来自正常小鼠的贴壁三硝基苯基衍生细胞则能够诱导该反应。利用紫外线处理的贴壁抗原呈递细胞在紫外线处理的小鼠中未能诱导免疫反应,这与抗原特异性抑制性T细胞的产生有关。本文讨论了这些结果对紫外线诱导致癌作用的意义。