免疫母亲所生小鼠中疟疾疫苗接种失败。
Failure of malaria vaccination in mice born to immune mothers.
作者信息
Harte P G, De Souza J B, Playfair J H
出版信息
Clin Exp Immunol. 1982 Sep;49(3):509-16.
Female BALB/c mice were vaccinated against blood stage P. yoelii (17XL strain), infected 2 weeks later and after recovery mated to normal C57B1/6 males. Control matings were with normal BALB/c females. The (C57B1/6 x BALB/c)F1 progeny were vaccinated at 4, 6, 8 or 10 weeks of age and infected 2 weeks later with lethal P. yoelii. All control mice were fully protected, but in the offspring of immune mothers mortality was 100, 87, 50, and 0% respectively. Mice in which the protective effect of vaccination had been abolished showed greatly reduced specific IgG and delayed hypersensitivity (DH) responses to challenge with parasite antigen. Results indicate that this failure of vaccination is due to the transmission of maternal IgG to the offspring which acts to suppress both priming by the vaccine and the generation of specific T helper cells involved in IgG production, as measured by the response to TNP-P. yoelii.
雌性BALB/c小鼠接种了约氏疟原虫血液期（17XL株）疫苗，2周后感染，恢复后与正常C57B1/6雄性小鼠交配。对照交配组采用正常BALB/c雌性小鼠。（C57B1/6×BALB/c）F1代子代在4、6、8或10周龄时接种疫苗，2周后用致死剂量的约氏疟原虫感染。所有对照小鼠均得到充分保护，但免疫母亲的子代死亡率分别为100%、87%、50%和0%。接种疫苗的保护作用已被消除的小鼠，其特异性IgG显著降低，对寄生虫抗原攻击的迟发型超敏反应（DH）延迟。结果表明，疫苗接种失败是由于母体IgG传递给子代，这抑制了疫苗引发的免疫反应以及参与IgG产生的特异性T辅助细胞的生成，这可通过对TNP-约氏疟原虫的反应来衡量。
Zotero 插件