Bendinelli M, Matteucci D, Toniolo A, Friedman H
Infect Immun. 1979 Apr;24(1):1-6. doi: 10.1128/iai.24.1.1-6.1979.
The ability of spleen cells of mice infected with oncornaviruses to depress the in vitro antibody responsiveness of normal lymphoid cells was exploited in an attempt to clarify the role played by the lymphatic leukemia virus (LLV) component in the immunodepressive properties of the Friend leukemia complex. Spleen cells of mice infected with LLV or, for comparison, with the entire complex were added to cultures of sheep erythrocyte-primed uninfected spleen cells, and the antibody-forming cells produced by the latter, after antigen restimulation, were assayed. The addition within 2 days from culture initiation of low numbers of cells infected with either virus preparation suppressed all stages of the response affecting the production of both immunoglobulin M and immunoglobulin G antibody. The activity of infected cells resisted doses of ultraviolet radiation which inhibit cell multiplication but was abolished by disrupting the cells and was prevented by the presence of anti-LLV antibodies. The LLV-infected spleen cells responsible for suppression were not removed by treatments which selectively remove or kill macrophages and exhibited surface properties of B lymphocytes. These results were interpreted as indicating that the effect is due to virus (or viral products) released by B cells. The suppressing cells in the spleens of mice in the early days of Friend leukemia complex infection presented superimposable properties, supporting the concept that their activity is also due to the LLV they release in large quantities. However, in later stages of infection, the spleens of Friend leukemia complex-infected mice also contained non-B-suppressing cells possibly derived from the proliferation of nonlymphoid LLV-producing cells caused by the neoplastic process.
利用感染肿瘤病毒的小鼠脾细胞抑制正常淋巴细胞体外抗体反应性的能力,试图阐明淋巴白血病病毒(LLV)成分在弗氏白血病复合体免疫抑制特性中所起的作用。将感染LLV的小鼠脾细胞,或作为对照,将感染整个复合体的小鼠脾细胞,加入用绵羊红细胞致敏的未感染脾细胞培养物中,并检测后者在抗原再刺激后产生的抗体形成细胞。在培养开始后2天内加入少量感染任一病毒制剂的细胞,可抑制影响免疫球蛋白M和免疫球蛋白G抗体产生的反应的所有阶段。感染细胞的活性能抵抗抑制细胞增殖的紫外线剂量,但通过破坏细胞可使其活性消失,且抗LLV抗体的存在可阻止其活性。负责抑制作用的LLV感染脾细胞不能通过选择性去除或杀死巨噬细胞的处理而被清除,且表现出B淋巴细胞的表面特性。这些结果被解释为表明该效应是由于B细胞释放的病毒(或病毒产物)所致。在弗氏白血病复合体感染早期,小鼠脾脏中的抑制细胞呈现出可叠加的特性,支持了它们的活性也是由于它们大量释放的LLV这一概念。然而,在感染后期,感染弗氏白血病复合体的小鼠脾脏中也含有可能源自肿瘤过程导致的非淋巴样LLV产生细胞增殖的非B抑制细胞。