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首页> 外文OA文献 >Virulent Salmonella enterica Serovar Typhimurium Evades Adaptive Immunity by Preventing Dendritic Cells from Activating T Cells
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Virulent Salmonella enterica Serovar Typhimurium Evades Adaptive Immunity by Preventing Dendritic Cells from Activating T Cells

机译：毒性沙门氏菌血清型鼠伤寒沙门氏菌通过阻止树突状细胞激活T细胞而逃避​​了适应性免疫。

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Dendritic cells (DCs) constitute the link between innate and adaptive immunity by directly recognizing pathogen-associated molecular patterns (PAMPs) in bacteria and by presenting bacterial antigens to T cells. Recognition of PAMPs renders DCs as professional antigen-presenting cells able to prime naïve T cells and initiate adaptive immunity against bacteria. Therefore, interfering with DC function would promote bacterial survival and dissemination. Understanding the molecular mechanisms that have evolved in virulent bacteria to evade activation of adaptive immunity requires the characterization of virulence factors that interfere with DC function. Salmonella enterica serovar Typhimurium, the causative agent of typhoid-like disease in the mouse, can prevent antigen presentation to T cells by avoiding lysosomal degradation in DCs. Here, we show that this feature of virulent Salmonella applies in vivo to prevent activation of adaptive immunity. In addition, this attribute of virulent Salmonella requires functional expression of a type three secretion system (TTSS) and effector proteins encoded within the Salmonella pathogenicity island 2 (SPI-2). In contrast to wild-type virulent Salmonella, mutant strains carrying specific deletions of SPI-2 genes encoding TTSS components or effectors proteins are targeted to lysosomes and are no longer able to prevent DCs from activating T cells in vitro or in vivo. SPI-2 mutant strains are attenuated in vivo, showing reduced tissue colonization and enhanced T-cell activation, which confers protection against a challenge with wild-type virulent Salmonella. Our data suggest that impairment of DC function by the activity of SPI-2 gene products is crucial for Salmonella pathogenesis.
机译：树突状细胞（DC）通过直接识别细菌中的病原体相关分子模式（PAMP）并将细菌抗原呈递给T细胞，从而在先天免疫和适应性免疫之间建立了联系。对PAMPs的识别使DCs成为能够提纯幼稚T细胞并启动针对细菌的适应性免疫的专业抗原呈递细胞。因此，干扰DC功能将促进细菌存活和传播。了解在毒性细菌中发展的分子机制以逃避适应性免疫的激活，需要表征干扰DC功能的毒力因子。鼠伤寒样鼠伤寒沙门氏菌血清型鼠伤寒沙门氏菌可通过避免DC的溶酶体降解来防止抗原呈递给T细胞。在这里，我们表明有毒的沙门氏菌的这一特征在体内适用于防止适应性免疫的激活。此外，强毒沙门氏菌的这一属性需要功能表达三型分泌系统（TTSS）和在沙门氏菌致病岛2（SPI-2）中编码的效应蛋白。与野生型强毒沙门氏菌相反，携带编码TTSS组分或效应蛋白的SPI-2基因特异性缺失的突变株被靶向溶酶体，并且不再能够阻止DC在体外或体内激活T细胞。 SPI-2突变株在体内减毒，显示出减少的组织定植和增强的T细胞活化，从而赋予了针对野生型强毒沙门氏菌的保护力。我们的数据表明，SPI-2基因产物的活性对DC功能的损害对于沙门氏菌的发病机理至关重要。

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