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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Immune complex-induced enhancement of bacterial antigen presentation requires Fcγ Receptor III expression on dendritic cells
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Immune complex-induced enhancement of bacterial antigen presentation requires Fcγ Receptor III expression on dendritic cells

机译：免疫复合物诱导的细菌抗原呈递增强需要树突状细胞上的Fcγ受体III表达

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Dendritic cells (DCs) are capable of initiating adaptive immune responses against infectious agents by presenting pathogen-derived antigens on MHC molecules to naieve T cells. Because of their key role in priming adaptive immunity, it is expected that interfering with DC function would be advantageous to the pathogen. We have previously shown that Salmonella enterica serovar Typhimurium (ST), is able to survive inside DCs and interfere with their function by avoiding activation of bacteria-specific T cells. In contrast, when ST is targeted to Fcγ receptors on the DC surface, bacteria are degraded and their antigens presented to T cells. However, the specific Fcγ receptor responsible of restoring presentation of antigens remains unknown. Here, we show that IgG-coated ST was targeted to lysosomes and degraded and its antigens presented on MHC molecules only when the low-affinity activating FcγRIII was expressed on DCs. FcγRIII-mediated enhancement of Ag presentation led to a robust activation of T cells specific for bacteria-expressed antigens. Laser confocal and electron microscopy analyses revealed that IgG-coated ST was rerouted to the lysosomal pathway through an FcγRIII-dependent mechanism. PI-3K activity was required for this process, because specific inhibitors promoted the survival of IgG-coated ST inside DCs and prevented DCs from activating bacteria-specific T cells. Our data suggest that the DC capacity to efficiently activate T cells upon capturing IgG-coated virulent bacteria is mediated by FcγRIII and requires PI-3K activity.
机译：树突状细胞（DC）能够通过将MHC分子上的病原体衍生抗原呈递给T细胞，从而启动针对传染原的适应性免疫反应。由于它们在引发适应性免疫中起关键作用，因此预期干扰DC功能将对病原体有利。先前我们已经表明，肠炎沙门氏菌鼠伤寒沙门氏菌（ST）能够在DC内部存活并通过避免细菌特异性T细胞的活化来干扰其功能。相反，当ST靶向DC表面上的Fcγ受体时，细菌被降解，其抗原呈递给T细胞。然而，负责恢复抗原呈递的特异性Fcγ受体仍然未知。在这里，我们表明，只有当低亲和力激活FcγRIII在DC上表达时，涂有IgG的ST才能靶向溶酶体并降解，其抗原呈递给MHC分子。 FcγRIII介导的Ag提呈增强导致特异于细菌表达抗原的T细胞活化。激光共聚焦和电子显微镜分析表明，包被IgG的ST通过FcγRIII依赖性机制重新路由至溶酶体途径。此过程需要PI-3K活性，因为特异性抑制剂可促进DC内IgG包被的ST的存活，并阻止DC激活细菌特异性T细胞。我们的数据表明，捕获IgG包被的毒性细菌后，DC有效激活T细胞的能力是由FcγRIII介导的，并且需要PI-3K活性。

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