Journal
NATURE MEDICINE
Volume 19, Issue 10, Pages 1273-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3284
Keywords
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Funding
- INSERM
- British Heart Foundation
- European Research Council
- Fondation Coeur et Recherche
- Fondation pour la Recherche Medicale
- European Union Seven Framework programme TOLERAGE
- Fondation Leducq Transatlantic Network
- US National Institutes of Health [AI56363, AI057157]
- Lymphoma Research Foundation
- Fondation pour la Recherche Medicale and from Journes de Biologie Clinique
- British Heart Foundation [PG/11/107/29236] Funding Source: researchfish
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Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6C(hi) monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell-selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction.
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