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Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells
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| Veröffentlicht in: | Frontiers in immunology 9(2018) Artikel-Nummer 1224, 12 Seiten |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| Titel: | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells/ Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
18 June 2018
|
| Gesamtaufnahme: |
: Frontiers in immunology, 9(2018) Artikel-Nummer 1224, 12 Seiten
, volume:9 |
| Schlagwörter: | |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 245 | 1 | 0 | |a Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells |c Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg |
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| 520 | |a Antigen presenting cells (APCs) regulate the balance of our immune response towards microbes. Whereas immunogenic APCs boost inflammation and activate lymphocytes, the highly plastic cells can switch into a tolerogenic/suppressive phenotype that dampens and resolves the response. Thereby the initially mediated inflammation seems to prime the switch of APCs while the strength of activation determines the grade of the suppressive phenotype. Recently we showed that pathogen recognition receptor-mediated pro-inflammatory cytokines reprogram differentiating human blood monocytes in vitro towards an immunosuppressive phenotype through prolonged activation of signal transducer and activator of transcription (STAT) 3. The TLR7/8 ligand R848 (Resiquimod) triggers the high release of cytokines from GM-CSF/IL-4-treated monocytes. These cytokines subsequently upregulate T cell suppressive factors, such as Programmed death-ligand 1 (PD-L1) and Indolamin-2,3-Dioxygenase (IDO) through cytokine receptor-mediated STAT3 activation. Here we reveal an essential role for the micro-RNA (miR) hsa-miR-99b/let-7e/miR-125a cluster in stabilizing the suppresive phenotype of R848-stimulated APCs on different levels. On the one hand the miR cluster boosts R848-stimulated cytokine production through regulation of MAPkinase inhibitor Tribbles homolog 2 (TRIB2), thereby enhancing cytokine-stimulated activation of STAT3. One the other hand, the STAT3 inhibitor suppressor of cytokine signaling-1 (SOCS1) is targeted by the miR cluster, stabilizing the STAT3-induced expression of immunosuppressive factors PD-L1 and IDO. Finally hsa-miR-99b/let-7e/miR-125a cluster regulates generation of the suppressive tryptophan (Trp) metabolite kynurenine by targeting the tryptophanyl-tRNA synthetase WARS, the direct competitor of IDO in terms of availability of Trp. In summary, our results reveal the hsa-miR99b/let-7e/miR-125a cluster as an important player in the concerted combination of mechanisms that stabilizes STAT3 activity and thus regulate R848-stimulated suppressive APCs. | ||
| 650 | 4 | |a hsa-miR-99b/ let-7e /miR-125a cluster | |
| 650 | 4 | |a IDO | |
| 650 | 4 | |a miRNA | |
| 650 | 4 | |a PD-L1 | |
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| 650 | 4 | |a suppressive APC | |
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| contents | Antigen presenting cells (APCs) regulate the balance of our immune response towards microbes. Whereas immunogenic APCs boost inflammation and activate lymphocytes, the highly plastic cells can switch into a tolerogenic/suppressive phenotype that dampens and resolves the response. Thereby the initially mediated inflammation seems to prime the switch of APCs while the strength of activation determines the grade of the suppressive phenotype. Recently we showed that pathogen recognition receptor-mediated pro-inflammatory cytokines reprogram differentiating human blood monocytes in vitro towards an immunosuppressive phenotype through prolonged activation of signal transducer and activator of transcription (STAT) 3. The TLR7/8 ligand R848 (Resiquimod) triggers the high release of cytokines from GM-CSF/IL-4-treated monocytes. These cytokines subsequently upregulate T cell suppressive factors, such as Programmed death-ligand 1 (PD-L1) and Indolamin-2,3-Dioxygenase (IDO) through cytokine receptor-mediated STAT3 activation. Here we reveal an essential role for the micro-RNA (miR) hsa-miR-99b/let-7e/miR-125a cluster in stabilizing the suppresive phenotype of R848-stimulated APCs on different levels. On the one hand the miR cluster boosts R848-stimulated cytokine production through regulation of MAPkinase inhibitor Tribbles homolog 2 (TRIB2), thereby enhancing cytokine-stimulated activation of STAT3. One the other hand, the STAT3 inhibitor suppressor of cytokine signaling-1 (SOCS1) is targeted by the miR cluster, stabilizing the STAT3-induced expression of immunosuppressive factors PD-L1 and IDO. Finally hsa-miR-99b/let-7e/miR-125a cluster regulates generation of the suppressive tryptophan (Trp) metabolite kynurenine by targeting the tryptophanyl-tRNA synthetase WARS, the direct competitor of IDO in terms of availability of Trp. In summary, our results reveal the hsa-miR99b/let-7e/miR-125a cluster as an important player in the concerted combination of mechanisms that stabilizes STAT3 activity and thus regulate R848-stimulated suppressive APCs. |
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| spelling | Hildebrand, Dagmar 1979- VerfasserIn (DE-588)1013137892 (DE-627)704967073 (DE-576)346073596 aut, Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg, 18 June 2018, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Published: 18 June 2018, Gesehen am 30.07.2018, Antigen presenting cells (APCs) regulate the balance of our immune response towards microbes. Whereas immunogenic APCs boost inflammation and activate lymphocytes, the highly plastic cells can switch into a tolerogenic/suppressive phenotype that dampens and resolves the response. Thereby the initially mediated inflammation seems to prime the switch of APCs while the strength of activation determines the grade of the suppressive phenotype. Recently we showed that pathogen recognition receptor-mediated pro-inflammatory cytokines reprogram differentiating human blood monocytes in vitro towards an immunosuppressive phenotype through prolonged activation of signal transducer and activator of transcription (STAT) 3. The TLR7/8 ligand R848 (Resiquimod) triggers the high release of cytokines from GM-CSF/IL-4-treated monocytes. These cytokines subsequently upregulate T cell suppressive factors, such as Programmed death-ligand 1 (PD-L1) and Indolamin-2,3-Dioxygenase (IDO) through cytokine receptor-mediated STAT3 activation. Here we reveal an essential role for the micro-RNA (miR) hsa-miR-99b/let-7e/miR-125a cluster in stabilizing the suppresive phenotype of R848-stimulated APCs on different levels. On the one hand the miR cluster boosts R848-stimulated cytokine production through regulation of MAPkinase inhibitor Tribbles homolog 2 (TRIB2), thereby enhancing cytokine-stimulated activation of STAT3. One the other hand, the STAT3 inhibitor suppressor of cytokine signaling-1 (SOCS1) is targeted by the miR cluster, stabilizing the STAT3-induced expression of immunosuppressive factors PD-L1 and IDO. Finally hsa-miR-99b/let-7e/miR-125a cluster regulates generation of the suppressive tryptophan (Trp) metabolite kynurenine by targeting the tryptophanyl-tRNA synthetase WARS, the direct competitor of IDO in terms of availability of Trp. In summary, our results reveal the hsa-miR99b/let-7e/miR-125a cluster as an important player in the concerted combination of mechanisms that stabilizes STAT3 activity and thus regulate R848-stimulated suppressive APCs., hsa-miR-99b/ let-7e /miR-125a cluster, IDO, miRNA, PD-L1, stat3, suppressive APC, Eberle, Mariel-Esther VerfasserIn (DE-588)1024722244 (DE-627)720417236 (DE-576)369401727 aut, Wölfle, Sabine J. VerfasserIn (DE-588)1132353580 (DE-627)887745903 (DE-576)488807026 aut, Falk, Franziska 1992- VerfasserIn (DE-588)1163560685 (DE-627)1027881769 (DE-576)508051509 aut, Sahin, Delal VerfasserIn (DE-588)1161034099 (DE-627)1024442136 (DE-576)506321886 aut, Sähr, Aline VerfasserIn (DE-588)1115378309 (DE-627)869766015 (DE-576)477779107 aut, Bode, Konrad A. 1969- VerfasserIn (DE-588)128891270 (DE-627)384629334 (DE-576)297385836 aut, Heeg, Klaus 1956- VerfasserIn (DE-588)133238369 (DE-627)539308587 (DE-576)299716805 aut, Enthalten in Frontiers in immunology Lausanne : Frontiers Media, 2010 9(2018) Artikel-Nummer 1224, 12 Seiten Online-Ressource (DE-627)657998354 (DE-600)2606827-8 (DE-576)343624834 1664-3224 nnns, volume:9 year:2018, http://dx.doi.org/10.3389/fimmu.2018.01224 Verlag Resolving-System kostenfrei Volltext, https://www.frontiersin.org/articles/10.3389/fimmu.2018.01224/full Verlag kostenfrei Volltext, http://dx.doi.org/10.3389/fimmu.2018.01224 LFER, LFER 2018-08-13T00:00:00Z |
| spellingShingle | Hildebrand, Dagmar, Eberle, Mariel-Esther, Wölfle, Sabine J., Falk, Franziska, Sahin, Delal, Sähr, Aline, Bode, Konrad A., Heeg, Klaus, Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells, Antigen presenting cells (APCs) regulate the balance of our immune response towards microbes. Whereas immunogenic APCs boost inflammation and activate lymphocytes, the highly plastic cells can switch into a tolerogenic/suppressive phenotype that dampens and resolves the response. Thereby the initially mediated inflammation seems to prime the switch of APCs while the strength of activation determines the grade of the suppressive phenotype. Recently we showed that pathogen recognition receptor-mediated pro-inflammatory cytokines reprogram differentiating human blood monocytes in vitro towards an immunosuppressive phenotype through prolonged activation of signal transducer and activator of transcription (STAT) 3. The TLR7/8 ligand R848 (Resiquimod) triggers the high release of cytokines from GM-CSF/IL-4-treated monocytes. These cytokines subsequently upregulate T cell suppressive factors, such as Programmed death-ligand 1 (PD-L1) and Indolamin-2,3-Dioxygenase (IDO) through cytokine receptor-mediated STAT3 activation. Here we reveal an essential role for the micro-RNA (miR) hsa-miR-99b/let-7e/miR-125a cluster in stabilizing the suppresive phenotype of R848-stimulated APCs on different levels. On the one hand the miR cluster boosts R848-stimulated cytokine production through regulation of MAPkinase inhibitor Tribbles homolog 2 (TRIB2), thereby enhancing cytokine-stimulated activation of STAT3. One the other hand, the STAT3 inhibitor suppressor of cytokine signaling-1 (SOCS1) is targeted by the miR cluster, stabilizing the STAT3-induced expression of immunosuppressive factors PD-L1 and IDO. Finally hsa-miR-99b/let-7e/miR-125a cluster regulates generation of the suppressive tryptophan (Trp) metabolite kynurenine by targeting the tryptophanyl-tRNA synthetase WARS, the direct competitor of IDO in terms of availability of Trp. In summary, our results reveal the hsa-miR99b/let-7e/miR-125a cluster as an important player in the concerted combination of mechanisms that stabilizes STAT3 activity and thus regulate R848-stimulated suppressive APCs., hsa-miR-99b/ let-7e /miR-125a cluster, IDO, miRNA, PD-L1, stat3, suppressive APC |
| swb_id_str | 508053064 |
| title | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells |
| title_auth | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells |
| title_full | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg |
| title_fullStr | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg |
| title_full_unstemmed | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg |
| title_in_hierarchy | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells / Dagmar Hildebrand, Mariel-Esther Eberle, Sabine Marie Wölfle, Franziska Egler, Delal Sahin, Aline Sähr, Konrad A. Bode and Klaus Heeg, |
| title_short | Hsa-miR-99b/let-7e/miR-125a cluster regulates pathogen recognition receptor-stimulated suppressive antigen-presenting cells |
| title_sort | hsa mir 99b let 7e mir 125a cluster regulates pathogen recognition receptor stimulated suppressive antigen presenting cells |
| topic | hsa-miR-99b/ let-7e /miR-125a cluster, IDO, miRNA, PD-L1, stat3, suppressive APC |
| topic_facet | hsa-miR-99b/ let-7e /miR-125a cluster, IDO, miRNA, PD-L1, stat3, suppressive APC |
| url | http://dx.doi.org/10.3389/fimmu.2018.01224, https://www.frontiersin.org/articles/10.3389/fimmu.2018.01224/full |