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TLR9 pathway is involved in adjuvant effects of plasmid DNA-based vaccines

机译：TLR9途径参与基于质粒DNA的疫苗的佐剂作用

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The presence of unmethylated CpG motifs in bacterial plasmids is thought to provide necessary immunoadjuvant signals to DNA vaccination. We took advantage of CpG-unresponsive toll-like receptor 9 (TLR9) knock-out mice to study whether this pathway was required to generate immune responses to DNA vaccination. We compared two vectors, one encoding the surface glycoprotein C of pseudorabies virus shown to protect target animals against challenge, and the other encoding the cytoplasmic enzyme beta-galactosidase. In the absence of TLR9, bone marrow-derived dendritic cells lost their ability to secrete IL-12 and type I IFN in response not only to CpG as expected but also to the plasmids used for vaccination. In contrast, DNA vaccination experiments showed that TLR9-deficient mice were able to mount Th1-biased antigen-specific antibody and IFN-gamma responses, albeit at lower levels than normal mice. Thus, TLR9 signaling is not needed for eliciting T- and B-cell responses to DNA encoded antigens. However, TLR9 signaling tended to enhance plasmid-adjuvant effects on antigen-specific immune responses.
机译：细菌质粒中未甲基化的CpG基序的存在被认为为DNA疫苗接种提供了必要的免疫佐剂信号。我们利用CpG无反应性的Toll样受体9（TLR9）敲除小鼠来研究是否需要这种途径来产生对DNA疫苗的免疫反应。我们比较了两种载体，一种编码伪狂犬病病毒的表面糖蛋白C，可保护目标动物免受攻击，另一种编码胞质酶β-半乳糖苷酶。在没有TLR9的情况下，源自骨髓的树突状细胞失去了分泌IL-12和I型IFN的能力，不仅响应了预期的CpG，还响应了用于疫苗接种的质粒。相比之下，DNA疫苗接种实验显示，尽管TLR9缺陷小鼠的水平低于正常小鼠，但它们能够引起Th1偏向的抗原特异性抗体和IFN-γ反应。因此，不需要TLR9信号来引发T细胞和B细胞对DNA编码抗原的反应。但是，TLR9信号转导倾向于增强对抗原特异性免疫反应的质粒佐剂作用。

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