Nickell S P, Freeman R R, Cole G A
Parasite Immunol. 1987 Mar;9(2):161-74. doi: 10.1111/j.1365-3024.1987.tb00497.x.
Mice with self-limiting P. yoelii or fatal P. berghei infections exhibited a markedly impaired ability to mount specific splenic cytotoxic T-lymphocyte responses to immunization with infectious ectromelia (EV), vaccinia (VAC), or lymphocytic choriomeningitis viruses (LCMV). Lymph node responsiveness, however, was not impaired. Primary CTL responses were depressed in mice immunized 7 days after P. berghei infection, while in P. yoelii-infected mice, depressed responses were detected only during the period corresponding with maximal parasitemia (days 9-12). Secondary VAC-specific CTL responses in vitro by spleen cells of mice previously immunized during P. yoelii infection were also depressed if UV-inactivated rather than infectious VAC was used for immunization. In addition, spleen cells of mice already immune to VAC failed to yield normal secondary CTL responses in vitro during the period of maximal P. yoelii parasitaemia. Collectively, these findings indicate that, during patent malaria infections, priming for and expression of virus-specific CTL responses may be inhibited.
感染自限性约氏疟原虫或致死性伯氏疟原虫的小鼠，对用传染性痘苗病毒（EV）、痘苗（VAC）或淋巴细胞性脉络丛脑膜炎病毒（LCMV）进行免疫接种产生特异性脾细胞毒性T淋巴细胞反应的能力显著受损。然而，淋巴结反应性并未受损。在感染伯氏疟原虫7天后免疫的小鼠中，原发性CTL反应受到抑制，而在感染约氏疟原虫的小鼠中，仅在与最大寄生虫血症相对应的时期（第9 - 12天）检测到反应受到抑制。如果用紫外线灭活而非传染性VAC进行免疫接种，在约氏疟原虫感染期间预先免疫的小鼠脾细胞在体外的继发性VAC特异性CTL反应也会受到抑制。此外，在约氏疟原虫最大寄生虫血症期间，已经对VAC免疫的小鼠脾细胞在体外未能产生正常的继发性CTL反应。总体而言，这些发现表明，在显性疟疾感染期间，病毒特异性CTL反应的启动和表达可能受到抑制。
