Escape of malaria parasites from host immunity requires CD4+CD25+ regulatory T cells

Escape of malaria parasites from host immunity requires CD4+CD25+ regulatory T cells
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DOI:
10.1038/nm975
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发表时间:
2004-01-01
期刊:
影响因子:
82.9
通讯作者:
Yasutomo, K
Yasutomo, K
中科院分区:
医学1区
文献类型:
--
作者:
Hisaeda, H;Maekawa, Y;Yasutomo, K

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疟原虫感染经常引起全面的免疫抑制,这使得宿主难以维持持久的免疫力。在这里,我们发现,当小鼠感染致命的约氏疟原虫菌株时,CD4(+)CD25(+)调节性T细胞(T-reg)的耗竭可以保护小鼠免于死亡,并且这种保护与T细胞对寄生虫源性抗原的反应性增强有关。这些结果表明,T-reg 细胞的激活有助于疟疾感染期间的免疫抑制,并帮助疟原虫逃避宿主的免疫反应。
Infection with malaria parasites frequently induces total immune suppression, which makes it difficult for the host to maintain long-lasting immunity. Here we show that depletion of CD4(+)CD25(+) regulatory T cells (T-reg) protects mice from death when infected with a lethal strain of Plasmodium yoelii, and that this protection is associated with an increased T-cell responsiveness against parasite-derived antigens. These results suggest that activation of T-reg cells contributes to immune suppression during malaria infection, and helps malaria parasites to escape from host immune responses.