Mancuso Giuseppe, Gambuzza Maria, Midiri Angelina, Biondo Carmelo, Papasergi Salvatore, Akira Shizuo, Teti Giuseppe, Beninati Concetta
The Elie Metchnikoff Department, University of Messina, Messina, Italy.
Nat Immunol. 2009 Jun;10(6):587-94. doi: 10.1038/ni.1733.
Little is known of how and where bacterial recognition triggers the induction of type I interferon. Whether the type of recognition receptor used in these responses is determined by the subcellular location of bacteria is not understood. Here we show that phagosomal bacteria such as group B streptococcus, but not cytosolic bacteria, potently induced interferon in conventional dendritic cells by a mechanism that required Toll-like receptor 7, the adaptor MyD88 and the transcription factor IRF1, all of which localized together with bacterial products in degradative vacuoles bearing lysosomal markers. Thus, this cell type-specific recognition pathway links lysosomal recognition of bacterial RNA with a robust, host-protective interferon response.
关于细菌识别如何以及在何处触发I型干扰素的诱导，人们知之甚少。这些反应中所使用的识别受体类型是否由细菌的亚细胞定位决定，目前尚不清楚。在这里，我们表明，诸如B族链球菌之类的吞噬体细菌，而非胞质细菌，通过一种需要Toll样受体7、衔接蛋白髓样分化因子88（MyD88）和转录因子干扰素调节因子1（IRF1）的机制，在传统树突状细胞中强烈诱导干扰素，所有这些都与带有溶酶体标记的降解性液泡中的细菌产物一起定位。因此，这种细胞类型特异性识别途径将细菌RNA的溶酶体识别与强大的宿主保护性干扰素反应联系起来。
