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Nat Med. 2013 Oct;19(10):1273-80. doi: 10.1038/nm.3284. Epub 2013 Sep 15.

B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction.

Author information

1
1] Institut National de la Santé et de la Recherche Médicale (INSERM), Unit 970, Paris Cardiovascular Research Center, Paris, France. [2] Université Paris-Descartes, Paris, France. [3].

Abstract

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.

PMID:
24037091
PMCID:
PMC4042928
DOI:
10.1038/nm.3284
[Indexed for MEDLINE]
Free PMC Article

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