Aims Recent studies have revealed that B cells and antibodies can influence inflammation
and remodelling following a myocardial infarction (MI) and culminating in heart failure—but …

Objectives: Here we assess the intrinsic functions of the chemokine receptor CXCR4 in
remodeling after myocardial infarction (MI) using Cxcr4 heterozygous (Cxcr4+/−) mice …

Background Mature B lymphocytes alter the recovery of cardiac function after acute
myocardial infarction (MI) in mice. Follicular B cells and marginal zone B (MZB) cells are …

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 …

A robust, sterile inflammation underlies myocardial ischemia and reperfusion injury (MIRI).
Several subsets of B cells possess the immunoregulatory capacity that limits tissue damage …

Acute coronary occlusion is the leading cause of death in the Western world. There is an
unmet need for the development of treatments to limit the extent of myocardial infarction (MI) …

Abstract Aims The CXC chemokine CXCL10 is up-regulated in the infarcted myocardium
and limits cardiac fibrosis by inhibiting growth factor-mediated fibroblast migration. CXCL10 …

Overactivated inflammatory responses contribute to adverse ventricular remodeling after
myocardial infarction (MI). Regulatory B cells (Bregs) are a newly discovered subset of B …

Background: Acute myocardial infarction (MI) elicits an inflammatory response that drives
tissue repair and adverse cardiac remodeling. Inflammatory cell trafficking after MI is …

Since the original descriptions of the role of stromal cell-derived factor (SDF)-1 in recruiting
bone marrow derived stem cells to the sites of vascular1 and myocardial injury, 2 there has …