Jayawardena A N, Targett G A, Leuchars E, Davies A J
Immunology. 1978 Jan;34(1):157-65.
CBA mice infected with the malaria parasite Plasmodium berghei yoelii (P. yoelii) develop a self-resolving infection lasting 15-18 days; on recovery from a primary infection they are immune to further infection. Cell and serum transfers from immune to non-immune mice were used to analyse the mechanism of resistance. Whereas serum from mice which had recovered from a single infection was ineffective in transferring immunity, hyperimmune serum (from mice repeatedly challenged with P. yoelii) protected against challenge inocula of 10(4) and 5 X 10(4) but was ineffective against higher inocula (10(5)). Doses of serum which completely protected intact mice were ineffective when administered to T-cell deprived recipients. The injection of spleen cells from recovered mice conferred immunity on both normal and T cell deprived mice. Pretreatment of immune cell donors with cyclophosphamide reduce the ability of spleen cells to transfer immunity. Treatment of the immune cells with an anti-Thy 1 antiserum and complement in vitro did not abrogate their protective effect. The significance of these results is discussed in relation to the effector mechanisms which might operate in murine malaria.
感染伯氏疟原虫约氏疟原虫（P. yoelii）的CBA小鼠会发展出一种持续15 - 18天的自限性感染；从初次感染恢复后，它们对进一步感染具有免疫力。通过将免疫小鼠的细胞和血清转移到非免疫小鼠来分析抗性机制。虽然单次感染恢复后的小鼠血清在转移免疫力方面无效，但超免疫血清（来自反复受到约氏疟原虫攻击的小鼠）可保护小鼠免受10⁴和5×10⁴个攻击接种物的感染，但对更高接种物（10⁵）无效。完全保护完整小鼠的血清剂量在给予T细胞缺失的受体时无效。注射来自恢复小鼠的脾细胞可使正常小鼠和T细胞缺失的小鼠都获得免疫力。用环磷酰胺预处理免疫细胞供体可降低脾细胞转移免疫力的能力。在体外使用抗Thy 1抗血清和补体处理免疫细胞并没有消除它们的保护作用。结合可能在鼠疟中起作用的效应机制对这些结果的意义进行了讨论。
