Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences, Radboud University, Nijmegen Medical Centre, Nijmegen, The Netherlands.
J Immunol. 2010 Feb 1;184(3):1280-91. doi: 10.4049/jimmunol.0900764. Epub 2009 Dec 28.
Chronic infections are caused by microorganisms that display effective immune evasion mechanisms. Dendritic cell (DC)-dependent T cell-mediated adaptive immunity is one of the mechanisms that have evolved to prevent the occurrence of chronic bacterial infections. In turn, bacterial pathogens have developed strategies to evade immune recognition. In this study, we show that gram-negative and gram-positive bacteria differ in their ability to activate DCs and that gram-negative bacteria are far more effective inducers of DC maturation. Moreover, we observed that only gram-negative bacteria can induce loss of adhesive podosome structures in DCs, a response necessary for the induction of effective DC migration. We demonstrate that the ability of gram-negative bacteria to trigger podosome turnover and induce DC migration reflects their capacity to selectively activate TLR4. Examining mice defective in TLR4 signaling, we show that this DC maturation and migration are mainly Toll/IL-1 receptor domain-containing adaptor-inducing IFNbeta-dependent. Furthermore, we show that these processes depend on the production of PGs by these DCs, suggesting a direct link between TLR4-mediated signaling and arachidonic metabolism. These findings demonstrate that gram-positive and gram-negative bacteria profoundly differ in their capacity to activate DCs. We propose that this inability of gram-positive bacteria to induce DC maturation and migration is part of the armamentarium necessary for avoiding the induction of an effective cellular immune response and may explain the frequent involvement of these pathogens in chronic infections.
慢性感染是由具有有效免疫逃避机制的微生物引起的。树突状细胞(DC)依赖性 T 细胞介导的适应性免疫是为了防止慢性细菌感染而进化出的机制之一。反过来,细菌病原体也发展出了逃避免疫识别的策略。在本研究中,我们表明革兰氏阴性菌和革兰氏阳性菌在激活 DC 的能力上存在差异,革兰氏阴性菌在诱导 DC 成熟方面更为有效。此外,我们观察到只有革兰氏阴性菌才能诱导 DC 中黏附足突结构的丧失,这是诱导有效 DC 迁移所必需的反应。我们证明革兰氏阴性菌触发足突周转和诱导 DC 迁移的能力反映了它们选择性激活 TLR4 的能力。检查 TLR4 信号传导缺陷的小鼠,我们表明这种 DC 成熟和迁移主要是 Toll/IL-1 受体结构域包含衔接子诱导 IFNβ 依赖的。此外,我们表明这些过程依赖于这些 DC 产生 PGs,表明 TLR4 介导的信号传导与花生四烯酸代谢之间存在直接联系。这些发现表明革兰氏阳性菌和革兰氏阴性菌在激活 DC 的能力上存在显著差异。我们提出,革兰氏阳性菌不能诱导 DC 成熟和迁移的能力是避免诱导有效细胞免疫反应所必需的武器库的一部分,这可能解释了这些病原体经常参与慢性感染的原因。