Cavacini L A, Long C A, Weidanz W P
Infect Immun. 1986 Jun;52(3):637-43. doi: 10.1128/iai.52.3.637-643.1986.
Acute infections caused by the murine malarial parasite Plasmodium chabaudi adami are resolved by antibody-independent mechanisms of immunity. The fact that athymic nude mice developed high-grade unrelenting malaria and died when infected with this parasite suggested a significant role for T lymphocytes. Using adoptive transfer techniques, we demonstrated that spleen cells from either nonimmune or immune donor BALB/c mice eventually suppressed P. chabaudi adami infections in histocompatible recipient nude mice in a dose-dependent manner. Infections in recipients of "immune" spleen cells were less severe, demonstrating a depressed peak parasitemia and a shortened duration of patent infection, than was observed in recipients of normal spleen cells. Also, when sufficient numbers of immune spleen cells were transferred, the second wave of parasitemia (characteristic of this infection in nonimmune mice) failed to occur. T lymphocytes mediated protection in recipient mice, since T-cell-enriched, but not B-cell-enriched, spleen cell fractions suppressed P. chabaudi adami infections in nude mice. Protection was best achieved with T cells that bore the L3T4 phenotype. Patent parasitemias developed in all recipient mice, suggesting that the grafted cells did not limit parasite growth directly but achieved this end by activating other as yet unidentified inhibiting cell systems.
由鼠疟原虫恰巴迪疟原虫亚当亚种引起的急性感染是通过非抗体免疫机制得以解决的。无胸腺裸鼠感染这种寄生虫后会患上严重且持续的疟疾并死亡，这一事实表明T淋巴细胞起着重要作用。利用过继转移技术，我们证明，来自非免疫或免疫供体BALB/c小鼠的脾细胞最终会以剂量依赖的方式抑制组织相容性受体裸鼠体内的恰巴迪疟原虫亚当亚种感染。与接受正常脾细胞的受体相比，接受“免疫”脾细胞的受体感染情况没那么严重，表现为寄生虫血症峰值降低且显性感染持续时间缩短。此外，当转移足够数量的免疫脾细胞时，第二波寄生虫血症（非免疫小鼠感染的特征）并未出现。T淋巴细胞介导受体小鼠的保护作用，因为富含T细胞而非富含B细胞的脾细胞组分可抑制裸鼠体内的恰巴迪疟原虫亚当亚种感染。具有L3T4表型的T细胞能最好地实现保护作用。所有受体小鼠均出现显性寄生虫血症，这表明移植的细胞并非直接限制寄生虫生长，而是通过激活其他尚未明确的抑制细胞系统来达到这一目的。
