Division of Cell Biology & Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Curr Opin Immunol. 2010 Feb;22(1):124-30. doi: 10.1016/j.coi.2009.12.005. Epub 2010 Jan 18.
Recent evidence suggests that TLR signalling in dendritic cells (DCs) transiently enhances antigen endocytosis and autophagy, augments the assembly of key antigen transport and processing systems, qualitatively modulates protein translation and induces a temporary cessation of DC motility. These rapid changes require activation of the MAP kinases, PI3-kinase and downstream signalling pathways and are observed in both myeloid DC and, with variations on the theme, in plasmacytoid DC.
最近的证据表明,树突状细胞(DC)中的 TLR 信号短暂增强了抗原内吞和自噬作用,增强了关键抗原运输和加工系统的组装,定性地调节了蛋白质翻译,并诱导 DC 运动的暂时停止。这些快速变化需要 MAP 激酶、PI3-激酶和下游信号通路的激活,并且在髓样 DC 中观察到,在浆细胞样 DC 中则存在主题上的变化。