Author
Listed:
- Marinos Kallikourdis
(Adaptive Immunity Laboratory, Humanitas Clinical and Research Center
Humanitas University)
- Elisa Martini
(Adaptive Immunity Laboratory, Humanitas Clinical and Research Center)
- Pierluigi Carullo
(Humanitas Clinical and Research Center
Institute of Genetic and Biomedical Research (IRGB)—UOS of Milan, National Research Council of Italy)
- Claudia Sardi
(Adaptive Immunity Laboratory, Humanitas Clinical and Research Center)
- Giuliana Roselli
(Adaptive Immunity Laboratory, Humanitas Clinical and Research Center)
- Carolina M. Greco
(Humanitas Clinical and Research Center)
- Debora Vignali
(Adaptive Immunity Laboratory, Humanitas Clinical and Research Center)
- Federica Riva
(Università degli Studi di Milano)
- Anne Marie Ormbostad Berre
(KG Jebsen Centre of Medicine, Norwegian University of Science and Technology)
- Tomas O. Stølen
(KG Jebsen Centre of Medicine, Norwegian University of Science and Technology
Norwegian Health Association)
- Andrea Fumero
(Cardiac Surgery, Humanitas Clinical and Research Center)
- Giuseppe Faggian
(University of Verona)
- Elisa Di Pasquale
(Humanitas Clinical and Research Center
Institute of Genetic and Biomedical Research (IRGB)—UOS of Milan, National Research Council of Italy)
- Leonardo Elia
(Humanitas Clinical and Research Center
University of Brescia)
- Cristiano Rumio
(Università degli Studi di Milano)
- Daniele Catalucci
(Institute of Genetic and Biomedical Research (IRGB)—UOS of Milan, National Research Council of Italy
Laboratory of Signal Transduction in Cardiac Pathologies, Humanitas Clinical and Research Center)
- Roberto Papait
(Humanitas Clinical and Research Center
Institute of Genetic and Biomedical Research (IRGB)—UOS of Milan, National Research Council of Italy)
- Gianluigi Condorelli
(Humanitas University
Humanitas Clinical and Research Center)
Abstract
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.
Suggested Citation
Marinos Kallikourdis & Elisa Martini & Pierluigi Carullo & Claudia Sardi & Giuliana Roselli & Carolina M. Greco & Debora Vignali & Federica Riva & Anne Marie Ormbostad Berre & Tomas O. Stølen & Andrea, 2017.
"T cell costimulation blockade blunts pressure overload-induced heart failure,"
Nature Communications, Nature, vol. 8(1), pages 1-14, April.
Handle:
RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14680
DOI: 10.1038/ncomms14680
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