Greenblatt H C, Potter T A, Rosenstreich D L
J Infect Dis. 1985 May;151(5):911-6. doi: 10.1093/infdis/151.5.911.
Inbred strains of mice differ greatly in their innate resistance to Trypanosoma rhodesiense, the etiologic agent of African sleeping sickness. BALB/c mice are very susceptible to this organism, whereas C57BL/6 mice are highly resistant. This difference is regulated by at least three distinct genes. An adoptive transfer study was performed in order to determine the tissue site of expression of these genes. Three inbred mouse strains (C57BL/6J, C3H.SW/SnJ, and BALB.B) that differ in resistance to T. rhodesiense, but are histocompatible at the H-2 locus, were used in the study. The adoptive transfer of normal bone marrow cells from C57BL/6J (resistant) mice into X-irradiated BALB.B (susceptible) mice rendered the recipient mice resistant to a subsequent experimental challenge with T. rhodesiense. Conversely, the transfer of bone marrow cells from BALB.B mice into irradiated C57BL/6J mice rendered the latter mice susceptible. Resistance could also be adoptively transferred from C57BL/6J mice to a second susceptible strain, C3H.SW/SnJ, by using either bone marrow or spleen cells. These findings demonstrate that although multiple genes control innate resistance to T. rhodesiense, all or most of these genes appear to control the development or function of cells whose progenitors reside in the spleen and bone marrow.
小鼠近交系对非洲昏睡病的病原体罗德西亚锥虫的先天抵抗力差异很大。BALB/c小鼠对这种病原体非常敏感，而C57BL/6小鼠则具有高度抗性。这种差异至少由三个不同的基因调控。为了确定这些基因的表达组织部位，进行了一项过继转移研究。研究中使用了三种对罗德西亚锥虫抵抗力不同但在H-2位点组织相容性相同的近交小鼠品系（C57BL/6J、C3H.SW/SnJ和BALB.B）。将C57BL/6J（抗性）小鼠的正常骨髓细胞过继转移到经X射线照射的BALB.B（敏感）小鼠中，使受体小鼠对随后的罗德西亚锥虫实验性攻击产生抗性。相反，将BALB.B小鼠的骨髓细胞转移到经照射的C57BL/6J小鼠中，使后者小鼠变得敏感。通过使用骨髓或脾细胞，抗性也可以从C57BL/6J小鼠过继转移到第二个敏感品系C3H.SW/SnJ。这些发现表明，尽管多个基因控制对罗德西亚锥虫的先天抵抗力，但所有或大多数这些基因似乎控制着祖细胞存在于脾脏和骨髓中的细胞的发育或功能。
