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Immunosuppression in murine malaria. III. Induction of tolerance and of immunological memory by soluble bovine serum albumin.

机译:鼠类疟疾的免疫抑制。三可溶性牛血清白蛋白诱导耐受性和免疫记忆。

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摘要

The primary antibody response to alumadsorbed BSA was depressed when initiated during low-grade chronic Plasmodium berghei malaria in mice, as previously reported during acute P.y. yoelii infection. Induction of immunological memory by soluble polymerized BSA was abolished in both infections; in infected hosts this normally immunogenic stimulus resulted in partial tolerance. In contrast to the depression of immune response, neither infection interfered with the induction of low-zone tolerance by monomeric BSA. The rate of non-immune elimination of BSA was found to be normal during acute malaria, and only slightly reduced in chronic infection. These results may be explained in terms of abnormal antigen handling in infected mice, due to some functional defect in macrophages, although this does not seem to be a sufficient explanation for all the phenomena of malaria-associated immunosuppression.
机译:如先前在急性P.y.中报道的那样,在小鼠低度慢性伯氏疟原虫疟疾期间启动时,对铝吸附的BSA的一抗反应受到抑制。 yoelii感染。两种感染都消除了可溶性聚合牛血清白蛋白对免疫记忆的诱导。在感染宿主中,这种通常具有免疫原性的刺激导致部分耐受。与降低免疫反应相反,这两种感染都不会干扰单体BSA诱导的低区耐受性。发现在急性疟疾期间非免疫消除BSA的速度是正常的,而在慢性感染中仅略有降低。这些结果可能是由于巨噬细胞中的某些功能缺陷引起的感染小鼠中异常抗原处理的结果,尽管这似乎不足以解释所有与疟疾相关的免疫抑制现象。

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