title: B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction.
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.
authors.affiliation: 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].
authors.forename: Yasmine
authors.initials: Y
authors.lastname: Zouggari
authors.forename: Hafid
authors.initials: H
authors.lastname: Ait-Oufella
authors.forename: Philippe
authors.initials: P
authors.lastname: Bonnin
authors.forename: Tabassome
authors.initials: T
authors.lastname: Simon
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Sage
authors.forename: Coralie
authors.initials: C
authors.lastname: Guérin
authors.forename: José
authors.initials: J
authors.lastname: Vilar
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Caligiuri
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Tsiantoulas
authors.forename: Ludivine
authors.initials: L
authors.lastname: Laurans
authors.forename: Edouard
authors.initials: E
authors.lastname: Dumeau
authors.forename: Salma
authors.initials: S
authors.lastname: Kotti
authors.forename: Patrick
authors.initials: P
authors.lastname: Bruneval
authors.forename: Israel F
authors.initials: IF
authors.lastname: Charo
authors.forename: Christoph J
authors.initials: CJ
authors.lastname: Binder
authors.forename: Nicolas
authors.initials: N
authors.lastname: Danchin
authors.forename: Alain
authors.initials: A
authors.lastname: Tedgui
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Tedder
authors.forename: Jean-Sébastien
authors.initials: JS
authors.lastname: Silvestre
authors.forename: Ziad
authors.initials: Z
authors.lastname: Mallat
mesh_terms: D000818:Animals; D053264:B-Cell Activating Factor / Q000097:blood; D001402:B-Lymphocytes / Q000378:metabolism / Q000502:physiology*; D054410:Chemokine CCL7 / Q000096:biosynthesis / Q000097:blood; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008212:Lymphocyte Depletion; D051379:Mice; D009000:Monocytes / Q000502:physiology*; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology*; D015398:Signal Transduction
chemical_list: D053264:B-Cell Activating Factor; C515451:Ccl7 protein, mouse; D054410:Chemokine CCL7; C505720:Tnfsf13b protein, mouse
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