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
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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DOI：
10.4049/jimmunol.176.9.5504
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发表时间：
2006-05-01
影响因子：
4.4
通讯作者：
Langhorne, Jean
中科院分区：
文献类型：
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作者：
Ndungu, Francis M.;Sanni, Latifu;Langhorne, Jean
我们研究了人CD 4 T细胞对恶性疟原虫红细胞膜蛋白-1的功能保守结构域半胱氨酸结构域间区-1 α（CIDR-1 α）的反应。对CIDR-1 α的反应是惊人的，因为暴露和未暴露的供体都有反应。IFN-γ对未暴露供体CIDR-1a的应答部分独立于MHC 11类和肽的TCR参与。相比之下，疟疾暴露供体中的CD 4 T细胞和IFN-γ应答是MHC II类限制性的，这表明疟疾半免疫成人中对CIDR-1 α的CD 4 T细胞应答也具有TCR介导的组分，这可能代表记忆应答。从人外周血中分离的树突状细胞被CIDR-1 α激活以产生IL-12、IL-10和IL-18。IL-12仅在培养的6和12小时之间可检测到，而IL-10在整个24小时的时间过程中继续增加。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-1a和宿主细胞之间的相互作用可能是负责调节CD 4 T细胞和细胞因子对恶性疟原虫感染的红细胞的反应。
We have studied the human CD4 T cell response to a functionally conserved domain of Plasmodium falciparum erythrocyte membrane protein-1, cysteine interdomain region-1 alpha (CIDR-1 alpha). Responses to CIDR-1 alpha were striking in that both exposed and nonexposed donors responded. The IFN-gamma response to CIDR-1a in the nonexposed donors was partially independent of TCR engagement of MHC class 11 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-1 alpha 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-1 alpha 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 A falciparum interacts directly with human dendritic cells, and suggests that the interaction between CIDR-1a and the host cell may be responsible for regulation of the CD4 T cell and cytokine responses to P. falciparum-infected erythrocytes reported previously.