title: Uncontrolled immune response in acute myocardial infarction: unraveling the thread.
abstract: Recently, the theory that hyperinflammation is the body's primary response to potent stimulus has been challenged. Indeed, a deregulation of the immune system could be the cause of multiple organ failure. So far, clinicians have focused on the last steps of the inflammatory cascade. However, little attention has been paid to lymphocytes, which play an important role as strategists of the inflammatory response. Experimental evidence suggests a crucial role of T lymphocytes in the pathophysiology of atherosclerosis and acute myocardial infarction (AMI). In summary, from the bottom of an imaginary inverted pyramid, a few regulatory T-cells control the upper parts represented by the wide spectrum of the inflammatory cascade. In AMI, a loss of regulation of the inflammatory system occurs in patients with a decreased activity of regulatory T-cells. As a consequence, aggressive T-cells boost and anti-inflammatory T-cells drop. A pleiotropic proinflammatory imbalance with damaging effects in terms of left ventricular performance and patient outcome is the result of this uncontrolled immune response. It is needed to unravel the thread of the inflammatory cells to better understand the pathophysiology as well as to open innovative therapeutic options in AMI.
authors.affiliation: Cardiology Department, Hospital Clinico Universitario, Valencia, Spain. vicentbodi@hotmail.com
authors.forename: Vicente
authors.initials: V
authors.lastname: Bodi
authors.forename: Juan
authors.initials: J
authors.lastname: Sanchis
authors.forename: Julio
authors.initials: J
authors.lastname: Nunez
authors.forename: Luis
authors.initials: L
authors.lastname: Mainar
authors.forename: Gema
authors.initials: G
authors.lastname: Minana
authors.forename: Isabel
authors.initials: I
authors.lastname: Benet
authors.forename: Carlos
authors.initials: C
authors.lastname: Solano
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Chorro
authors.forename: Angel
authors.initials: A
authors.lastname: Llacer
mesh_terms: D000818:Animals; D001324:Autoantigens / Q000276:immunology; D016207:Cytokines / Q000097:blood; D004562:Electrocardiography; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007964:Leukocytosis / Q000276:immunology; D018655:Lymphocyte Count; D051379:Mice; D009000:Monocytes / Q000276:immunology; D009102:Multiple Organ Failure / Q000276:immunology; D009203:Myocardial Infarction / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D011379:Prognosis; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D018487:Ventricular Dysfunction, Left / Q000276:immunology
chemical_list: D001324:Autoantigens; D016207:Cytokines; D018836:Inflammation Mediators