Weinbaum F I, Evans C B, Tigelaar R E
J Immunol. 1976 Nov;117(5 Pt.2):1999-2005.
The course of infection with 17X nonlethal Plasmodium berghei yoelii was examined in BALB/c mice which were deficient in either T cells or B cells. Markedly increased parasitemia and mortality were observed in athymic (nude) mice which had been backcrossed on a BALB/c background (T cell deficient) compared to similar mice which had been grafted with neonatal BALB/c thymus, and were also observed in BALB/c mice suppressed from birth with goat antiserum to mouse mu-chain (B cell deficient) compared to age- and sex-matched BALB/c controls. These results establish the requirement for the presence of both T cells and B cells for effective resistance to an intercurrent infection with 17XNL P.b. yoelii in adult BALB/c mice. Mechanisms by which the requirement for both T cells and B cells could be explained were discussed. The model of mu suppression was shown to be a valuable tool for an evaluation of the cellular basis of immunity to an infectious disease.
在T细胞或B细胞缺陷的BALB/c小鼠中,研究了感染17X非致死性约氏疟原虫的病程。与移植了新生BALB/c胸腺的类似小鼠相比,在以BALB/c为背景回交的无胸腺(裸)小鼠(T细胞缺陷)中观察到明显更高的寄生虫血症和死亡率,并且与年龄和性别匹配的BALB/c对照相比,在用山羊抗小鼠μ链血清从出生起就受到抑制的BALB/c小鼠(B细胞缺陷)中也观察到了这种情况。这些结果证实了成年BALB/c小鼠有效抵抗17XNL约氏疟原虫并发感染需要同时存在T细胞和B细胞。讨论了解释T细胞和B细胞两者需求的机制。μ抑制模型被证明是评估传染病免疫细胞基础的一个有价值的工具。