Mattsson D M, Howard R J, Balfour H H
Infect Immun. 1980 Dec;30(3):700-8. doi: 10.1128/iai.30.3.700-708.1980.
Splenic lymphocytes from cytomegalovirus-infected mice lost their in vitro proliferative responses to cytomegalovirus antigen within 3 h after in vivo treatment with antilymphocyte globulin and prednisolone. The response was inhibited when the agents were administered separately or together, and inhibition persisted through a 2-week course of immunosuppression. Circulating specific antibodies were depressed by multiple injections of antilymphocyte globulin alone or with prednisolone, but not by prednisolone alone. Mitogen-induced blast transformation was immediately depressed by immunosuppression with both agents. Although the response to lipopolysaccharide returned briefly, it declined with continuing treatment. Cytomegalovirus infection augmented the depressive effect of immunosuppression on the lipopolysaccharide proliferative response. Prednisolone treatment of infected animals did not affect the concanavalin A response, and lipopolysaccharide stimulation decreased more slowly and to a lesser extent than it did in mice treated with antilymphocyte globulin or both agents. Loss of specific cell-mediated immunity and simultaneous depression of humoral immunity indicated that immunosuppression immediately created an inability to respond to an active cytomegalovirus infection.
在用抗淋巴细胞球蛋白和泼尼松龙进行体内治疗后3小时内，来自巨细胞病毒感染小鼠的脾淋巴细胞丧失了其对巨细胞病毒抗原的体外增殖反应。当单独或联合给予这些药物时，反应均受到抑制，并且抑制作用在为期2周的免疫抑制疗程中持续存在。单独多次注射抗淋巴细胞球蛋白或与泼尼松龙联合注射可降低循环特异性抗体水平，但单独使用泼尼松龙则无此作用。两种药物进行免疫抑制可立即抑制有丝分裂原诱导的母细胞转化。尽管对脂多糖的反应短暂恢复，但随着持续治疗而下降。巨细胞病毒感染增强了免疫抑制对脂多糖增殖反应的抑制作用。对感染动物进行泼尼松龙治疗不影响其对刀豆球蛋白A的反应，并且与用抗淋巴细胞球蛋白或两种药物治疗的小鼠相比，脂多糖刺激的下降更缓慢且程度更小。特异性细胞介导免疫的丧失和体液免疫的同时抑制表明，免疫抑制立即导致无法对活跃的巨细胞病毒感染作出反应。
