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Macrophage cytotoxicity in lethal and non-lethal murine malaria and the effect of vaccination.

机译:致命和非致命鼠类疟疾中的巨噬细胞细胞毒性和疫苗接种作用。

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摘要

We investigated the development of cell-mediated immunity in lethal and non-lethal malarial infections by assaying the cytotoxic activity of spleen cells for L929 tumour cells at different times after infection of mice with the lethal P. berghei, a lethal variant of Plasmodium yoelii and the non-lethal P. yoelii and P. chabaudi. In all cases the cytotoxicity increased to a peak during the first week and then diminished but the time of the peak varied with the infection; its activity was lowest with P. berghei. A second peak occurred in the non-lethal infections at the time of recovery. A protective vaccine accelerated and enhanced the early peak of cytotoxicity. The activity was mediated by adherent phagocytic cells, probably through the release of tumour necrosis factor (TNF) by macrophages since it was inhibited by antiserum against recombinant mouse TNF and did not destroy TNF-resistant L929 cells. Its induction was not dependent on T cells since it occurred in T cell-deficient mice infected with non-lethal P. yoelii. However, the accelerated increase associated with vaccination could be adoptively transferred by spleen lymphocytes from vaccinated mice.
机译:我们通过在致死性伯氏疟原虫,约氏疟原虫和致死性疟原虫的致死变体感染小鼠后的不同时间分析脾细胞对L929肿瘤细胞的细胞毒性活性,研究了致死性和非致死性疟疾感染中细胞介导的免疫的发展。非致死性的约氏疟原虫和恰巴迪氏体育。在所有情况下,细胞毒性在第一个星期都增加到一个峰值,然后减弱,但是峰值时间随感染而变化;其活性在伯氏疟原虫中最低。恢复时非致死性感染出现第二个高峰。保护性疫苗加速并增强了细胞毒性的早期高峰。该活性是由粘附的吞噬细胞介导的,可能是通过巨噬细胞释放肿瘤坏死因子(TNF)引起的,因为该活性被针对重组小鼠TNF的抗血清所抑制,并且没有破坏TNF抗性的L929细胞。它的诱导不依赖于T细胞,因为它发生在感染了非致命约氏疟原虫的T细胞缺陷小鼠中。但是,与疫苗接种有关的加速增加可以由接种小鼠的脾淋巴细胞过继转移。

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