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首页> 外文OA文献 >CD4 T cells from malaria-nonexposed individuals respond to the CD36-Binding Domain of Plasmodium falciparum erythrocyte membrane protein-1 via an MHC class II-TCR-independent pathway.
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CD4 T cells from malaria-nonexposed individuals respond to the CD36-Binding Domain of Plasmodium falciparum erythrocyte membrane protein-1 via an MHC class II-TCR-independent pathway.

机译：来自未感染疟疾的个体的CD4 T细胞通过MHC II类-TCR非依赖性途径应答恶性疟原虫红细胞膜蛋白1的CD36结合域。

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摘要

We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1alpha (CIDR-1alpha). Responses to CIDR-1alpha were striking in that both exposed and nonexposed donors responded. The IFN-gamma response to CIDR-1alpha in the nonexposed donors was partially independent of TCR engagement of MHC class II and peptide. Contrastingly, CD4 T cell and IFN-gamma responses in malaria-exposed donors were MHC class II restricted, suggesting that the CD4 T cell response to CIDR-1alpha in malaria semi-immune adults also has a TCR-mediated component, which may represent a memory response. Dendritic cells isolated from human peripheral blood were activated by CIDR-1alpha to produce IL-12, IL-10, and IL-18. IL-12 was detectable only between 6 and 12 h of culture, whereas the IL-10 continued to increase throughout the 24-h time course. These data strengthen previous observations that P. falciparum interacts directly with human dendritic cells, and suggests that the interaction between CIDR-1alpha and the host cell may be responsible for regulation of the CD4 T cell and cytokine responses to P. falciparum-infected erythrocytes reported previously.
机译：我们已经研究了人类CD4 T细胞对功能保守的恶性疟原虫红细胞膜蛋白1域，半胱氨酸域间区域1alpha（CIDR-1alpha）的反应。对CIDR-1alpha的反应令人惊讶，因为暴露的和未暴露的供体都做出了反应。在未暴露的供体中对CIDR-1alpha的IFN-γ反应部分独立于II类MHC和肽的TCR参与。相反，疟疾暴露供体中的CD4 T细胞和IFN-γ反应受到MHC II类限制，这表明疟疾半免疫成年人中对CIDR-1alpha的CD4 T细胞反应也具有TCR介导的成分，这可能代表了记忆反应。从人类外周血中分离的树突状细胞被CIDR-1alpha激活以产生IL-12，IL-10和IL-18。 IL-12仅在培养的6至12小时之间可检测到，而IL-10在整个24小时的过程中持续增加。这些数据加强了以前关于恶性疟原虫直接与人树突状细胞相互作用的观察结果，并表明CIDR-1alpha与宿主细胞之间的相互作用可能是CD4 T细胞的调节和细胞因子对恶性疟原虫感染的红细胞反应的报道。先前。

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