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首页> 外文期刊>Infection and immunity >Host defenses in murine malaria: evaluation of the mechanisms of immunity to Plasmodium yoelii infection.
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Host defenses in murine malaria: evaluation of the mechanisms of immunity to Plasmodium yoelii infection.

机译:鼠类疟疾的宿主防御:对约氏疟原虫感染的免疫机制的评估。

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The immune response of random-bred mice to infection with a relatively avirulent strain of Plasmodium yoelii was measured in terms of parasitemia, splenomegaly, immediate and delayed hypersensitivity to a P. yoelii antigen preparation, resistance to challenge with a virulent variant of P. yoelii, and nonspecific resistance to L. monocytogenes. Avirulent P. yoelii produced a self limiting infection which resolved in 21 days. Peak parasitemia and splenomegaly were observed at 14 days, and infected mice were resistant to challenge with virulent P. yoelii from 7 days through at least 126 days. Mice infected with avirulent P. yoelii developed humoral immunity as judged by immediate hypersensitivity reactions and the capacity of their serum to passively protect normal mice against virulent P. yoelii. At no time did mice infected with the avirulent P. yoelii display evidence of cell-mediated immunity, as expressed by delayed-type hypersensitivity and increased resistance to L. monocytogenes. In fact, at the height of avirulent P. yoelii infection there was decreased resistance to L. monocytogenes in both liver and spleen, and the macrophages of the undisturbed peritoneal cavity were similarly defective. It was concluded that the defense mechanism of mice against P. yoelii is mediated by humoral factors in the absence of demonstrable cell-mediated immunity.
机译:根据寄生虫血症,脾肿大,对约耶氏疟原虫抗原制剂的超敏反应,对约氏疟原虫的强毒株的攻击抵抗性,测量了随机繁殖的小鼠对相对无毒力的约氏疟原虫菌株感染的免疫反应。 ,以及对单核细胞增生李斯特菌的非特异性抗性。无毒的约氏疟原虫产生了一种自我限制的感染,该感染在21天内得到解决。在第14天观察到了最高的寄生虫血症和脾肿大,并且受感染的小鼠在7天到至少126天期间对强毒的约氏疟原虫具有抗性。通过立即的超敏反应及其血清被动保护正常小鼠免受强毒性约氏疟原虫的能力判断,感染无毒的约氏疟原虫的小鼠会产生体液免疫。感染无毒的约氏疟原虫的小鼠在任何时候都没有表现出细胞介导的免疫力的证据,这表现为迟发型超敏反应和对单核细胞增生李斯特氏菌的抗性增强。实际上,在无毒的约氏疟原虫感染高峰期,肝脏和脾脏中对单核细胞增生李斯特氏菌的抵抗力均下降,并且未受干扰的腹膜腔巨噬细胞同样具有缺陷。结论是,在缺乏可证明的细胞介导的免疫力的情况下,体液因子介导了小鼠对约氏疟原虫的防御机制。

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