Campbell G H, Esser K M, Weinbaum F I
Infect Immun. 1977 Nov;18(2):434-8. doi: 10.1128/iai.18.2.434-438.1977.
B-cell-deficient C57B1/6J mice (suppressed from birth with goat anti-mu) and controls (treated from birth with normal goat serum) were infected with Trypanosoma rhodesiense. There was a significant (P less than 0.01) decrease in duration of survival of the mu-suppressed mice compared with that of controls. Whereas both mu-suppressed and control mice had an initial rise in parasitemia of similar magnitude, only the control mice exhibited a subsequent period during which the parasitemia fell to undetectable levels. In control mice, immunization with irradiated organisms prevented the development of detectable parasitemia after challenge with viable trypanosomes. However, immunization did not alter the course of infection in B-cell-deficient mice. These results indicate that immunity to T. rhodesiense infection in mice is dependent on B-cell immunocompetence.
用羊抗μ链抗体从出生起就进行抑制的B细胞缺陷型C57B1/6J小鼠和对照组(从出生起用正常山羊血清处理)感染了罗德西亚锥虫。与对照组相比,μ链抑制的小鼠存活时间显著缩短(P<0.01)。虽然μ链抑制的小鼠和对照小鼠的寄生虫血症最初都有相似程度的升高,但只有对照小鼠随后出现了寄生虫血症降至无法检测水平的时期。在对照小鼠中,用经辐照的生物体进行免疫可防止在用活锥虫攻击后出现可检测到的寄生虫血症。然而,免疫并没有改变B细胞缺陷型小鼠的感染进程。这些结果表明,小鼠对罗德西亚锥虫感染的免疫力依赖于B细胞免疫能力。