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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Toll-like Receptor Ligands Synergize Through Distinct Dendritic Cell Pathways To Induce T Cell Responses: Implications For Vaccines
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Toll-like Receptor Ligands Synergize Through Distinct Dendritic Cell Pathways To Induce T Cell Responses: Implications For Vaccines

机译：Toll样受体配体通过不同的树突状细胞途径协同诱导T细胞反应：对疫苗的影响。

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摘要

Toll-like receptors (TLRs) may need to cooperate with each other to be effective in detecting imminent infection and trigger immune responses. Understanding is still limited about the intracellular mechanism of this cooperation. We found that when certain TLRs are involved, dendritic cells (DCs) establish unidirectional intracellular cross-talk, in which the MyD88-independent TRIF-dependent pathway amplifies the MyD88-dependent DC function through a JNK-dependent mechanism. The amplified MyD88-dependent DC function determines the induction of the T cell response to a given vaccine in vivo. Therefore, our study revealed an underlying TLR mechanism governing the functional, nonrandom interplay among TLRs for recognition of combinatorial ligands that may be dangerous to the host, providing important guidance for design of novel synergistic molecular vaccine adjuvants.
机译：Toll样受体（TLR）可能需要相互配合才能有效检测即将到来的感染并触发免疫反应。对这种合作的细胞内机制的了解仍然有限。我们发现，当涉及某些TLR时，树突状细胞（DC）建立单向细胞内串扰，其中MyD88独立的TRIF依赖性途径通过JNK依赖性机制放大了MyD88依赖性DC功能。扩增的依赖MyD88的DC功能决定了体内T细胞对特定疫苗反应的诱导。因此，我们的研究揭示了一种潜在的TLR机制，该机制控制着TLR之间的功能性，非随机性相互作用，以识别可能对宿主造成危险的组合配体，为新型协同分子疫苗佐剂的设计提供重要指导。

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