Recognition of molecular signatures of potential pathogens via toll-like receptors (TLRs) activates dendritic cells (DC), leading to the initiation of adaptive immunity. TLR signalling in DC causes an increase in display of MHC peptide ligands for T cell recognition, upregulation of co-stimulatory molecules important for T cell clonal expansion and secretion of immunomodulatory cytokines, which direct T cell differentiation into effectors. Remarkably, ligation of distinct TLRs can trigger differential cytokine production in a single DC type or result in different cytokines in distinct DC sub-types. Studying the complexity of DC responses to TLR ligands illuminates the link between innate recognition and adaptive immunity, paving the way for improved vaccines and strategies to induce tolerance to autoantigens or allografts.

中文翻译：

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Toll样受体和树突状细胞：虫子为之收费。

通过通行费样受体（TLR）识别潜在病原体的分子标记可激活树突状细胞（DC），从而导致适应性免疫的启动。DC中的TLR信号传导会增加THC识别的MHC肽配体的显示，对T细胞克隆扩增和免疫调节细胞因子的分泌很重要的共刺激分子的上调，这将T细胞分化为效应子。值得注意的是，不同TLR的连接可以触发单一DC类型中差异性的细胞因子产生，或导致不同DC亚型中不同的细胞因子。对DC对TLR配体的反应的复杂性的研究阐明了先天识别与适应性免疫之间的联系，为改进疫苗和诱导对自身抗原或同种异体耐受的策略铺平了道路。