Cunningham D S, Kuhn R E, Rowland E C
Infect Immun. 1978 Oct;22(1):155-60. doi: 10.1128/iai.22.1.155-160.1978.
C57BL/6 mice exhibit low parasitemias and often survive Trypanosoma cruzi infections, whereas C3H(He) mice die during the acute phase with relatively high parasitemias. The present study showed that both strains of mice develop nonspecific immunosuppression to challenge with sheep erythrocytes during the course of infection. Several major differences in immunosuppression-related phenomena between the two strains of mice were determined, yet there is no apparent relationship between immunosuppression and resistance to T. cruzi. Both the number of direct plaque-forming cells and the titer of 2-mercaptoethanol-sensitive agglutinating antibody were significantly lower on day 11 for C57BL/6 mice and day 9 for C3H(He) mice. The number of indirect plaque-forming cells and the titer of mercaptoethanol-resistant agglutinating antibody were reduced by day 36 of infection in C57BL/6 mice and 13 days postinfection in C3H(He) mice. In both strains the degree of humoral response suppression of mice increased concomitant with the period of infection, but was not correlated with the changes in spleen cell numbers. Preliminary experiments designed to explore the mechanism underlying the induction and maintenance of immunosuppression in this hostparasite model disclosed the presence of suppressor substance in the serum of T. cruzi-infected mice. The passive transfer of serum from infected mice to syngeneic recipients elicited a state of immunosuppression to sheep erythrocytes, but did not diminish anti-erythrocyte activity in allogeneic recipients. The induction of immunosuppression in normal mice was further found to be dependent on the interval between serum transfer and challenge with antigen. No quantitative differences existed between the magnitude of suppressed humoral responses in mice infected for varying lengths of time and recipients of serum collected from similarly infected mice.
C57BL/6小鼠的寄生虫血症较低,通常能在感染克氏锥虫后存活,而C3H(He)小鼠在急性期会因较高的寄生虫血症而死亡。本研究表明,这两种品系的小鼠在感染过程中都会对绵羊红细胞的攻击产生非特异性免疫抑制。确定了两种品系小鼠在免疫抑制相关现象上的几个主要差异,但免疫抑制与对克氏锥虫的抵抗力之间没有明显关系。C57BL/6小鼠在第11天和C3H(He)小鼠在第9天,直接空斑形成细胞数量和2-巯基乙醇敏感凝集抗体效价均显著降低。在C57BL/6小鼠感染后第36天和C3H(He)小鼠感染后13天,间接空斑形成细胞数量和巯基乙醇抗性凝集抗体效价降低。在这两个品系中,小鼠体液反应抑制程度均随感染时间延长而增加,但与脾细胞数量变化无关。旨在探索该宿主-寄生虫模型中免疫抑制诱导和维持机制的初步实验揭示,克氏锥虫感染小鼠血清中存在抑制物质。将感染小鼠的血清被动转移至同基因受体可引发对绵羊红细胞的免疫抑制状态,但不会降低异基因受体中的抗红细胞活性。进一步发现,正常小鼠中免疫抑制的诱导取决于血清转移与抗原攻击之间的间隔时间。在不同时间感染的小鼠和从类似感染小鼠收集血清的受体中,体液反应抑制程度的大小不存在定量差异。