Neutrophils scan for activated platelets to initiate inflammation.
Neutrophils scan for activated platelets to initiate inflammation.
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DOI：
10.1126/science.1256478
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发表时间：
2014-12-05
期刊：
影响因子：
--
通讯作者：
Hidalgo A
中科院分区：
文献类型：
--
作者：
Sreeramkumar V;Adrover JM;Ballesteros I;Cuartero MI;Rossaint J;Bilbao I;Nácher M;Pitaval C;Radovanovic I;Fukui Y;McEver RP;Filippi MD;Lizasoain I;Ruiz-Cabello J;Zarbock A;Moro MA;Hidalgo A
免疫和炎症反应需要白细胞在脉管系统内迁移并通过脉管系统迁移，这一过程通过白细胞切换到受体不对称分布的极化形态的能力来促进。我们报告说，活化的小静脉内的中性粒细胞极化有助于组织一个突出的结构域，该结构域与血流中存在的活化的血小板结合。选择素配体 PSGL-1 转导这些相互作用发出的信号，导致驱动中性粒细胞迁移的受体重新分布。因此，无法极化或通过 PSGL-1 转导信号的中性粒细胞表现出异常爬行，而阻断该结构域可以保护小鼠免受血栓炎症损伤。这些结果揭示了募集的中性粒细胞扫描活化的血小板，并表明它们的双极性允许在炎症发生之前整合内皮和循环中存在的信号。
Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thrombo-inflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and suggest that their bipolarity allows integration of signals present at both the endothelium and the circulation before inflammation proceeds.
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DOI：
10.1084/jem.20112322
发表时间：
2012-04-09
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
von Brühl ML;Stark K;Steinhart A;Chandraratne S;Konrad I;Lorenz M;Khandoga A;Tirniceriu A;Coletti R;Köllnberger M;Byrne RA;Laitinen I;Walch A;Brill A;Pfeiler S;Manukyan D;Braun S;Lange P;Riegger J;Ware J;Eckart A;Haidari S;Rudelius M;Schulz C;Echtler K;Brinkmann V;Schwaiger M;Preissner KT;Wagner DD;Mackman N;Engelmann B;Massberg S
通讯作者：
Massberg S
影响因子：
82.9
作者：
Phillipson M;Kubes P
通讯作者：
Kubes P
影响因子：
7.8
作者：
Kunisaki, Yuya;Nishikimi, Akihiko;Tanaka, Yoshihiko;Takii, Ryosuke;Noda, Mayuko;Inayoshi, Ayumi;Watanabe, Ken-ichi;Sanematsu, Fumiyuki;Sasazuki, Takehiko;Sasaki, Takehiko;Fukui, Yoshinori
通讯作者：
Fukui, Yoshinori
影响因子：
15.9
作者：
Caudrillier, Axelle;Kessenbrock, Kai;Looney, Mark R.
通讯作者：
Looney, Mark R.
影响因子：
48
作者：
Chiang, Elaine Y.;Hidalgo, Andres;Frenette, Paul S.
通讯作者：
Frenette, Paul S.