| Literature DB >> 24037091 |
Yasmine Zouggari1, Hafid Ait-Oufella, Philippe Bonnin, Tabassome Simon, Andrew P Sage, Coralie Guérin, José Vilar, Giuseppina Caligiuri, Dimitrios Tsiantoulas, Ludivine Laurans, Edouard Dumeau, Salma Kotti, Patrick Bruneval, Israel F Charo, Christoph J Binder, Nicolas Danchin, Alain Tedgui, Thomas F Tedder, Jean-Sébastien Silvestre, Ziad Mallat.
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.Entities:
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Year: 2013 PMID： 24037091 PMCID： PMC4042928 DOI： 10.1038/nm.3284
Source DB: PubMed Journal: Nat Med ISSN： 1078-8956 Impact factor: 53.440