A Bcl-2-dependent molecular timer regulates the lifespan and immunogenicity of dendritic cells
A Bcl-2-dependent molecular timer regulates the lifespan and immunogenicity of dendritic cells
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DOI：
10.1038/ni1071
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发表时间：
2004-06-01
影响因子：
30.5
通讯作者：
Van Parijs, L
中科院分区：
文献类型：
--
作者：
Hou, WS;Van Parijs, L
携带抗原的树突状细胞（DC）的寿命由来自病原体和T细胞的信号决定。这些信号通过调节Bcl-2家族蛋白的表达来调节DC存活。Toll样受体和T细胞共刺激分子均触发依赖于Bcl-x（L）的DC存活途径。然而，Toll样受体独特地增加Bim的表达并通过被Bcl-2阻断的途径触发细胞死亡。该通路作为分子“计时器”，其设定DC的寿命并调节体内T细胞应答的大小。因此，来自先天性和获得性免疫系统的信号通过不同的分子机制控制DC寿命和免疫原性。
The lifespan of antigen-bearing dendritic cells (DCs) is determined by signals from pathogens and T cells. These signals regulate DC survival by modulating expression of Bcl-2 family proteins. Toll-like receptors and T cell costimulatory molecules both trigger a DC survival pathway that is dependent on Bcl-x(L). However, Toll-like receptors uniquely increase expression of Bim and trigger cell death by a pathway that is blocked by Bcl-2. This pathway serves as a molecular 'timer' that sets the lifespan of DCs and regulates the magnitude of T cell responses in vivo. Thus, signals derived from the innate and acquired immune systems control DC lifespan and immunogenicity by distinct molecular mechanisms.