Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway

Sudan He; Yuqiong Liang; Feng Shao; Xiaodong Wang

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Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway

机译：Toll样受体通过受体相互作用激酶3介导的途径激活巨噬细胞中的程序性坏死

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We report here that mouse macrophages undergo receptor-interacting kinase-3 (RIP3)-dependent but TNF-ct-independent necrosis when Toll-like receptors (TLR) 3 and 4 are activated by poly(I:C) and LPS, respectively. An adaptor protein, Toll/IL-1 receptor domain-containing adapter inducing IFN-β (TRIF/TICAM-1), which is dispensable for TNF-α-induced necrosis, forms a complex with RIP3 upon TLR3/ TLR4 activation and is essential forTLR3/TLR4-induced necrosis. Mice without RIP3 or functional TRIF did not show macrophage loss and elevation of inflammatory cytokines when they were exposed to LPS. Necrosis in mouse macrophages induced by either TNFR or TLR3/TLR4 is executed by reactive oxygen species. Taken together, these data indicate that there are multiple upstream necrosis-initiating signaling pathways converging on the RIP3 during an innate immune response to viral and bacterial infections in mammals.

机译：我们在这里报告说，当Toll样受体（TLR）3和4分别被poly（I：C）和LPS激活时，小鼠巨噬细胞会经历受体相互作用激酶3（RIP3）依赖性但TNF-ct依赖性坏死。配体蛋白，包含Toll / IL-1受体域的配体诱导IFN-β（TRIF / TICAM-1），可用于TNF-α诱导的坏死，在TLR3 / TLR4激活后与RIP3形成复合物，这是必不可少的forTLR3 / TLR4诱导的坏死。当小鼠暴露于LPS时，没有RIP3或功能性TRIF的小鼠没有显示巨噬细胞丢失和炎性细胞因子升高。 TNFR或TLR3 / TLR4诱导的小鼠巨噬细胞坏死是由活性氧引起的。综上所述，这些数据表明在哺乳动物对病毒和细菌感染的先天免疫应答过程中，RIP3上存在多个上游坏死启动信号通路。

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《Proceedings of the National Academy of Sciences of the United States of America》 |2011年第50期|p.20054-20059|共6页
作者
Sudan He; Yuqiong Liang; Feng Shao; Xiaodong Wang;
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作者单位

CyrusTang Hematology Center, Jiangsu Institute of Hematology, First Affiliated Hospital, Soochow University, Suzhou 215123, China;

National Institute of Biological Sciences, Beijing 102206, China;

National Institute of Biological Sciences, Beijing 102206, China;

National Institute of Biological Sciences, Beijing 102206, China;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类
关键词
necroptosis; bone marrow-derived macrophage;

机译：坏死骨髓巨噬细胞;

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1. Toll-like receptor 4-mediated ROS signaling pathway involved in Ganoderma atrum polysaccharide-induced tumor necrosis factor-alpha secretion during macrophage activation [J] . Qiang Yu, Shao-Ping Nie, Jun-Qiao Wang, Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research . 2014,第Null期

机译：Toll样受体4介导的ROS信号通路参与巨噬细胞活化过程中灵芝多糖诱导的肿瘤坏死因子-α分泌。
2. SNO-MLP (S-Nitrosylation of Muscle LIM Protein) Facilitates Myocardial Hypertrophy Through TLR3 (Toll-Like Receptor 3)–Mediated RIP3 (Receptor-Interacting Protein Kinase 3) and NLRP3 (NOD-Like Receptor Pyrin Domain Containing 3) Inflammasome Activation [J] . Xin Tang, Lihong Pan, Shuang Zhao, Circulation: An Official Journal of the American Heart Association . 2020,第12期

机译：通过TLR3（Toll样受体3）介导的RIP3（受体相互作用蛋白激酶3）和NLRP3（含有3个）炎症组的NOR样受体吡林结构域的NLRP3（含有3）炎症组的NLRP3（含有3）炎症组活化的NLRP3（含有3）氨基激活的NLRP3（含有3）活化
3. Mycobacterium tuberculosis Rv0652 stimulates production of tumour necrosis factor and monocytes chemoattractant protein-1 in macrophages through the Toll-like receptor 4 pathway [J] . KimK., SohnH., KimJ.-S., Immunology: An Official Journal of the British Society for Immunology . 2012,第2期

机译：结核分枝杆菌Rv0652通过Toll样受体4途径刺激巨噬细胞中肿瘤坏死因子和单核细胞趋化蛋白1的产生
4. Protein-protein interaction network of toll-like receptor 4 in macrophages with exposure to their agonists and external factors [C] . Abu Hena M. Kamal, Jayanta K. Chakrabarty, Saiful M. Chowdhury ASMS Conference on Mass Spectrometry and Allied Topics . 2016

机译：巨噬蛋白 - 蛋白质相互作用网络在巨噬细胞中暴露于其激动剂和外部因素
5. The function, activation and inhibition of phosphatidic acid phosphohydrolase-1 and Group IVA phospholipase A2 in toll-like receptor-4 activated macrophages. [D] . Grkovich, Andrej. 2008

机译：Toll样受体4活化巨噬细胞中磷脂酸磷酸水解酶1和IVA组磷脂酶A2的功能，激活和抑制。
6. Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway [O] . Sudan He, Yuqiong Liang, Feng Shao, 2011

机译：Toll样受体通过受体相互作用激酶3介导的途径激活巨噬细胞中的程序性坏死
7. Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway [O] . He, Sudan, Liang, Yuqiong, Shao, Feng, 2011

机译：Toll样受体通过受体相互作用激酶3介导的途径激活巨噬细胞中的程序性坏死

Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3-mediated pathway

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