Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, USA.
Immunol Rev. 2010 Mar;234(1):163-76. doi: 10.1111/j.0105-2896.2009.00867.x.
Plasmacytoid dendritic cells (pDCs) are specialized dendritic cells (DCs) that produce large amounts of type I interferon (IFN) after Toll-like receptor (TLR) activation. Human pDCs preferentially express immunoglobulin-like transcript 7 (ILT7; LILRA4), which couples with a signaling adapter to activate a prominent immunoreceptor tyrosine-based activation motif (ITAM)-mediated signaling pathway. ILT7 protein directly binds to and can be activated by bone marrow stromal cell antigen 2 (BST2; CD317) protein, the expression of which is found on cells pre-exposed to IFN or on the surface of human cancer cells. The interaction between ILT7 and BST2 functions to assure an appropriate TLR response by pDCs during viral infection and likely participates in pDC-tumor crosstalk. Two opposing modes of receptor-mediated regulatory mechanisms work jointly to fine tune the innate immunity of pDCs.
浆细胞样树突状细胞 (pDCs) 是一种特化的树突状细胞 (DCs)，在 Toll 样受体 (TLR) 激活后会产生大量的 I 型干扰素 (IFN)。人类 pDCs 优先表达免疫球蛋白样转录物 7 (ILT7; LILRA4)，它与信号适配器结合，激活一个显著的免疫受体酪氨酸基激活基序 (ITAM) 介导的信号通路。ILT7 蛋白直接结合并可被骨髓基质细胞抗原 2 (BST2; CD317) 蛋白激活，该蛋白在预先暴露于 IFN 的细胞或人类癌细胞表面表达。ILT7 和 BST2 之间的相互作用可确保 pDCs 在病毒感染期间对 TLR 做出适当的反应，并且可能参与 pDC-肿瘤串扰。两种相反的受体介导的调节机制模式共同作用，精细调节 pDCs 的先天免疫。
