Suzuki Y, Watanabe N, Kobayashi A
Infect Immun. 1981 Oct;34(1):36-42. doi: 10.1128/iai.34.1.36-42.1981.
The effect of Toxoplasma infection on initiation and expression of memory cells to dinitrophenol (DNP)-conjugated protein antigens in humoral immune responses was studied in mice. Marked suppression in the initiation of memory cells to DNP-conjugated keyhole limpet hemocyanin occurred in the acute phase of infection. However, once the memory cells were induced before infection, expression of the memory cells was not affected. Moreover, the suppression of priming occurred on both T and B cells. The suppressive effect was observed in all immunoglobulin classes tested, i.e., immunoglobulin M (IgM), IgG1, IgG2, and IgE, regardless of the four kinds of DNP-conjugated protein antigens. This nonspecific suppression could be induced only by living toxoplasmas, by either the peroral or parenteral route, but not by lysed organisms. A transfer of normal spleen cells could not restore the ability of infected mice to initiate memory cells. Furthermore, the suppressive effect of the infected mice was not removed by 400 R of gamma-irradiation. These results suggested that irradiation-resistant suppressor cells cause nonspecific suppression of the initiation of memory cells in Toxoplasma-infected mice.
在小鼠中研究了弓形虫感染对体液免疫应答中针对二硝基苯酚（DNP）结合蛋白抗原的记忆细胞启动和表达的影响。在感染急性期，针对DNP结合的钥孔戚血蓝蛋白的记忆细胞启动受到明显抑制。然而，一旦在感染前诱导出记忆细胞，记忆细胞的表达就不受影响。此外，启动的抑制发生在T细胞和B细胞上。在所有测试的免疫球蛋白类别中，即免疫球蛋白M（IgM）、IgG1、IgG2和IgE，无论四种DNP结合蛋白抗原如何，均观察到抑制作用。这种非特异性抑制仅可由活的弓形虫通过口服或肠胃外途径诱导产生，而不能由裂解的生物体诱导产生。正常脾细胞的转移不能恢复感染小鼠启动记忆细胞的能力。此外，400伦琴的γ射线照射不能消除感染小鼠的抑制作用。这些结果表明，抗辐射抑制细胞对弓形虫感染小鼠中记忆细胞的启动产生非特异性抑制。
