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T cell costimulation blockade blunts pressure overload-induced heart failure.

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Kallikourdis M,Martini E,Carullo P,Sardi C,Roselli G,Greco CM,Vignali D,Riva F,Ormbostad Berre AM,Stølen TO,Fumero A,Faggian G,Di Pasquale E,Elia L,Rumio C,Catalucci D,Papait R,Condorelli G

doi

10.1038/ncomms14680

subject

Has Abstract

pub_date

2017-03-06 00:00:00

pages

14680

issn

2041-1723

pii

ncomms14680

journal_volume

8

pub_type

杂志文章

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