دورية أكاديمية
T cell costimulation blockade blunts pressure overload-induced heart failure
العنوان: | T cell costimulation blockade blunts pressure overload-induced heart failure |
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المؤلفون: | Kallikourdis, Marinos, Martini, Elisa, Carullo, Pierluigi, Sardi, Claudia, Roselli, Giuliana, Greco, Carolina M, Vignali, Debora, Riva, Federica, Berre, Anne Marie Ormbostad, Stølen, Tomas, Fumero, Andrea, Faggian, Giuseppe, Di Pasquale, Elisa, Elia, Leonardo, Rumio, Cristiano, Catalucci, Daniele, Papait, Roberto, Condorelli, Gianluigi |
المصدر: | 8 ; Nature Communications |
بيانات النشر: | Nature Publishing Group |
سنة النشر: | 2017 |
المجموعة: | NTNU Open Archive (Norges teknisk-naturvitenskapelige universitet / Norwegian University of Science and Technology) |
الوصف: | Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patients. T cell costimulation blockade, through FDA-approved rheumatoid arthritis drug abatacept, leads to highly significant delay in progression and decreased severity of cardiac dysfunction in the mouse HF model. The therapeutic effect occurs via inhibition of activation and cardiac infiltration of T cells and macrophages, leading to reduced cardiomyocyte death. Abatacept treatment also induces production of anti-inflammatory cytokine interleukin-10 (IL-10). IL-10-deficient mice are refractive to treatment, while protection could be rescued by transfer of IL 10-sufficient B cells. These results suggest that T cell costimulation blockade might be therapeutically exploited to treat HF. ; publishedVersion ; © The Author(s). 2017.This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0Test/ |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | application/pdf |
اللغة: | English |
تدمد: | 2041-1723 |
العلاقة: | Nature Communications. 2017, 8.; urn:issn:2041-1723; http://hdl.handle.net/11250/2503089Test; https://doi.org/10.1038/ncomms14680Test; cristin:1505825 |
DOI: | 10.1038/ncomms14680 |
الإتاحة: | https://doi.org/10.1038/ncomms14680Test http://hdl.handle.net/11250/2503089Test |
حقوق: | Navngivelse 4.0 Internasjonal ; http://creativecommons.org/licenses/by/4.0/deed.noTest |
رقم الانضمام: | edsbas.D8D5ED01 |
قاعدة البيانات: | BASE |
تدمد: | 20411723 |
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DOI: | 10.1038/ncomms14680 |