Sizemore R C, Mansfield J M
Cell Immunol. 1984 Dec;89(2):439-44. doi: 10.1016/0008-8749(84)90345-9.
The immunosuppression that occurs in mice experimentally infected with African trypanosomiasis has been examined further. In the present study we have examined lymph node cells from Trypanosoma rhodesiense-infected C57Bl/6J mice for the ability to produce mitogen induced antigen-nonspecific suppressor T cells (Ts). Inguinal, mesenteric, and brachial lymph node cells were harvested from uninfected control mice and from mice at different periods of infection. These cells were cultured with or without concanavalin A (Con A) for 48 hr to induce Ts activity. After stimulation, the control and infected lymph node cells were passed over Sephadex G-10 columns to remove suppressor macrophages that arise during the infection from Con A-induced Ts. The column passed cells were then added to normal mouse responder spleen cells in a primary in vitro antibody response culture system with sheep erythrocytes (SRBC) as antigen. The resultant plaque-forming cell responses to SRBC indicated that Ts function was not induced in infected lymph node cell populations. However, early in the infection, a stimulatory signal was provided by both the untreated and Con A-treated infected lymph node cells, which was lost in the terminal stage. Determinations of T cell subpopulations revealed that the infected Lyt 2.2-bearing subpopulation was not significantly altered from normal controls. We conclude that T. rhodesense infected mice fail to mount normal lymph node cell antigen nonspecific Ts responses and that this loss of activity may be due to an intrinsic dysfunction in the suppressor T cell population.
对实验感染非洲锥虫病的小鼠所发生的免疫抑制进行了进一步研究。在本研究中,我们检测了感染罗德西亚锥虫的C57Bl/6J小鼠的淋巴结细胞产生丝裂原诱导的抗原非特异性抑制性T细胞(Ts)的能力。从未感染的对照小鼠以及处于不同感染阶段的小鼠中采集腹股沟、肠系膜和肱部淋巴结细胞。将这些细胞在有或无刀豆球蛋白A(Con A)的情况下培养48小时以诱导Ts活性。刺激后,将对照和感染的淋巴结细胞通过Sephadex G - 10柱,以去除感染期间从Con A诱导的Ts中产生的抑制性巨噬细胞。然后将通过柱的细胞添加到以绵羊红细胞(SRBC)为抗原的原代体外抗体反应培养系统中的正常小鼠反应性脾细胞中。对SRBC产生的噬斑形成细胞反应表明,在感染的淋巴结细胞群体中未诱导出Ts功能。然而,在感染早期,未处理和Con A处理的感染淋巴结细胞均提供了刺激信号,而在末期该信号消失。T细胞亚群的测定显示,感染的携带Lyt 2.2的亚群与正常对照相比没有显著变化。我们得出结论,感染罗德西亚锥虫的小鼠无法产生正常的淋巴结细胞抗原非特异性Ts反应,这种活性丧失可能归因于抑制性T细胞群体的内在功能障碍。