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001     130541
005     20240228143442.0
024 7 _ |a 10.1080/2162402X.2016.1204506
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024 7 _ |a 2162-402X
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037 _ _ |a DKFZ-2017-05620
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Sektioglu, Ibrahim M
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245 _ _ |a Macrophage-derived nitric oxide initiates T-cell diapedesis and tumor rejection.
260 _ _ |a Austin, Tex.
|c 2016
|b Landes Bioscience
336 7 _ |a article
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520 _ _ |a In tumor biology, nitric oxide (NO) is generally regarded as an immunosuppressive molecule that impedes T-cell functions and activation of endothelial cells. Contrasting with this view, we here describe a critical role for NO derived from inducible nitric oxide (iNOS)-expressing tumor macrophages in T-cell infiltration and tumor rejection as shown by iNOS gene deletion, inhibition of iNOS, or NO donors. Specifically, macrophage-derived NO was found to induce on tumor vessels adhesion molecules that were required for T-cell extravasation. Experiments with human endothelial cells revealed a bimodal dose-dependent effect of NO. High doses of NO donors were indeed suppressive but lower, more physiological concentrations, induced adhesion molecules in an NFkB-dependent pathway and preferentially activated transcription of genes involved in lymphocyte diapedesis. iNOS(+) macrophages in tumors appear to generate precisely the amount of NO that promotes endothelial activation and T-cell infiltration. These results will be valuable for the development of strategies designed to overcome the paucity of T-cell infiltration into tumors that is a major obstacle in clinical cancer immunotherapy.
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700 1 _ |a Carretero, Rafael
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700 1 _ |a Bender, Noemi
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700 1 _ |a Bogdan, Christian
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700 1 _ |a Garbi, Natalio
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700 1 _ |a Umansky, Viktor
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700 1 _ |a Umansky, Ludmila
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700 1 _ |a Urban, Katharina
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700 1 _ |a Knebel Döberitz, Christina
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700 1 _ |a Somasundaram, Veena
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700 1 _ |a Wink, David
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700 1 _ |a Beckhove, Philipp
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700 1 _ |a Hämmerling, Günter
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773 _ _ |a 10.1080/2162402X.2016.1204506
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