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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >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的反应令人震惊，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MHC II类和肽的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。这些数据加强了先前的观察，即恶性疟原虫直接与人树突状细胞相互作用，并表明CIDR-1alpha与宿主细胞之间的相互作用可能是调节CD4 T细胞和细胞因子对恶性疟原虫感染的红细胞的反应的报道。先前。

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