Toll-like receptors induce a phagocytic gene program through p38.
Toll-like receptors induce a phagocytic gene program through p38.
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DOI：
10.1084/jem.20031237
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发表时间：
2004-01-05
期刊：
影响因子：
--
通讯作者：
Cheng G
中科院分区：
文献类型：
--
作者：
Doyle SE;O'Connell RM;Miranda GA;Vaidya SA;Chow EK;Liu PT;Suzuki S;Suzuki N;Modlin RL;Yeh WC;Lane TF;Cheng G
Toll样受体（TLR）信号传导和吞噬作用是巨噬细胞介导的对细菌感染的先天免疫应答的标志。然而，这两个过程之间的关系并没有很好地建立。我们的数据表明，TLR配体特异性地促进细菌的吞噬作用，在小鼠和人类细胞，通过诱导的吞噬基因程序。重要的是，TLR诱导的细菌吞噬作用被发现依赖于髓样分化因子88依赖性信号传导，通过白细胞介素-1受体相关激酶-4和p38导致清道夫受体的上调。有趣的是，单个TLR在不同程度上促进吞噬作用，其中TLR 9是最强的，TLR 3是该过程的最弱诱导剂。我们还表明，TLR配体不仅放大吞噬细胞摄取大肠杆菌的百分比，而且增加单个巨噬细胞吞噬的细菌数量。总之，我们的数据描述了一种进化上保守的机制，通过这种机制，TLR可以在感染期间特异性地促进细菌的吞噬清除。
Toll-like receptor (TLR) signaling and phagocytosis are hallmarks of macrophage-mediated innate immune responses to bacterial infection. However, the relationship between these two processes is not well established. Our data indicate that TLR ligands specifically promote bacterial phagocytosis, in both murine and human cells, through induction of a phagocytic gene program. Importantly, TLR-induced phagocytosis of bacteria was found to be reliant on myeloid differentiation factor 88–dependent signaling through interleukin-1 receptor–associated kinase-4 and p38 leading to the up-regulation of scavenger receptors. Interestingly, individual TLRs promote phagocytosis to varying degrees with TLR9 being the strongest and TLR3 being the weakest inducer of this process. We also demonstrate that TLR ligands not only amplify the percentage of phagocytes uptaking Escherichia coli, but also increase the number of bacteria phagocytosed by individual macrophages. Taken together, our data describe an evolutionarily conserved mechanism by which TLRs can specifically promote phagocytic clearance of bacteria during infection.
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影响因子：
32.4
作者：
Kawai, T;Adachi, O;Akira, S
通讯作者：
Akira, S
影响因子：
56.9
作者：
MULLER, U;STEINHOFF, U;AGUET, M
通讯作者：
AGUET, M
影响因子：
64.8
作者：
Alexopoulou, L;Holt, AC;Flavell, RA
通讯作者：
Flavell, RA
DOI：
10.1084/jem.180.2.705
发表时间：
1994-08-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
de Villiers WJ;Fraser IP;Hughes DA;Doyle AG;Gordon S
通讯作者：
Gordon S
影响因子：
32.4
作者：
Doyle, SE;Vaidya, SA;Cheng, G
通讯作者：
Cheng, G