T cell costimulation blockade blunts pressure overload-induced heart failure View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-03-06

AUTHORS

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 Fumero, Giuseppe Faggian, Elisa Di Pasquale, Leonardo Elia, Cristiano Rumio, Daniele Catalucci, Roberto Papait, Gianluigi Condorelli

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. More... »

PAGES

14680

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms14680

    DOI

    http://dx.doi.org/10.1038/ncomms14680

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1084128908

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28262700


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