Yasumoto S, Hayashi Y, Aurelian L
Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore 21201.
J Immunol. 1987 Oct 15;139(8):2788-93.
Ultraviolet B irradiation (280 to 320 nm) of mice at the site of intradermal infection with herpes simplex virus type 2 increased the severity of the herpes simplex virus type 2 disease and decreased delayed-type hypersensitivity (DTH) responses to viral antigen. Decrease in DTH resulted from the induction of suppressor T cells, as evidenced by the ability of spleen cells from UV-irradiated mice to inhibit DTH and proliferative responses after adoptive transfer. Lymph node cells from UV-irradiated animals did not transfer suppression. DTH was suppressed at the induction but not the expression phase. Suppressor T cells were Lyt-1+, L3T4+, and their activity was antigen-specific. However, after in vitro culture of spleen cells from UV-irradiated mice with herpes simplex virus type 2 antigen, suppressor activity was mediated by Lyt-2+ cells. Culture supernatants contained soluble nonantigen-specific suppressive factors.
用2型单纯疱疹病毒对小鼠进行皮内感染，然后对感染部位进行紫外线B（280至320纳米）照射，会加重2型单纯疱疹病毒疾病的严重程度，并降低对病毒抗原的迟发型超敏反应（DTH）。DTH的降低是由抑制性T细胞的诱导所致，这一点可通过紫外线照射小鼠的脾细胞在过继转移后抑制DTH和增殖反应的能力得到证明。紫外线照射动物的淋巴结细胞不能传递抑制作用。DTH在诱导阶段而非表达阶段受到抑制。抑制性T细胞为Lyt-1+、L3T4+，其活性具有抗原特异性。然而，用2型单纯疱疹病毒抗原体外培养紫外线照射小鼠的脾细胞后，抑制活性由Lyt-2+细胞介导。培养上清液含有可溶性非抗原特异性抑制因子。
