title: Lymphocyte Communication in Myocardial Ischemia/Reperfusion Injury.
abstract: CONCLUSIONS
  Myocardial ischemia/reperfusion (I/R) is an important complication of reperfusion therapy for myocardial infarction (MI). It is a complex process involving metabolic and immunological factors. To date, no effective treatment has been identified. Recent Advances: Previous research has focused on the role of innate immune cells in I/R injury. In recent years, increasing evidence has accumulated for an important role for adaptive immune cells, particularly T lymphocytes. Data from ST elevation MI patients have identified prognostic significance for lymphocyte counts, particularly postreperfusion lymphopenia. Dynamic changes in circulating CD4+T cell subsets occurring early after reperfusion are associated with development of I/R injury in the form of microvascular obstruction. Transcoronary gradients in cell counts suggest sequestration of these cells into the reperfused myocardium. These findings support existing data from mouse models indicating a role for CD4+T cells in I/R injury. It is clear, however, the effects of lymphocytes in the ischemic myocardium are time and subset specific, with some having protective effects, while others are pathogenic.
  
  
  RESULTS
  An understanding of the cellular events that lead to accumulation of lymphocytes in the myocardium, and their actions once there, is key to manipulating this process. Chemokines produced in response to ischemia and cellular injury have an important role, while lymphocyte-derived cytokines are critical in the balance between inflammation and healing.
  
  
  CONCLUSIONS
  Further research into the involvement of lymphocytes in myocardial I/R injury may allow development of targeted therapies, opening a new avenue of considerable therapeutic potential. Antioxid. Redox Signal. 26, 660-675.
authors.affiliation: 1 Institute of Genetic Medicine, Newcastle University , Newcastle upon Tyne, United Kingdom .|2 Regional Department of Clinical Immunology, Royal Victoria Infirmary, Newcastle upon Tyne, United Kingdom .
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Boag
authors.affiliation: 1 Institute of Genetic Medicine, Newcastle University , Newcastle upon Tyne, United Kingdom .
authors.forename: Emanuele
authors.initials: E
authors.lastname: Andreano
authors.affiliation: 1 Institute of Genetic Medicine, Newcastle University , Newcastle upon Tyne, United Kingdom .
authors.forename: Ioakim
authors.initials: I
authors.lastname: Spyridopoulos
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology; D006801:Humans; D051379:Mice; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000276:immunology* / Q000473:pathology; D009206:Myocardium / Q000276:immunology / Q000473:pathology
keywords: T cells; adaptive immunity; inflammation; ischemia/reperfusion injury; lymphocytes; myocardial infarction