Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study

J Vasc Res. 2024;61(5):260-266. doi: 10.1159/000541069. Epub 2024 Sep 18.

Abstract

Introduction: In ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear.

Methods: We examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls.

Results: Our findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar.

Conclusion: CD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.

Keywords: CD4+CD28null; Immune senescence; Inflammation; Myocardial infarction; T cells.

Publication types

  • News

MeSH terms

  • Aged
  • CD28 Antigens* / metabolism
  • CD4 Lymphocyte Count
  • CD4-Positive T-Lymphocytes* / immunology
  • CD4-Positive T-Lymphocytes* / metabolism
  • Case-Control Studies
  • Cellular Senescence
  • Coronary Circulation*
  • Coronary Sinus
  • Cytokines* / blood
  • Cytokines* / metabolism
  • Female
  • Humans
  • Immunophenotyping
  • Inflammation Mediators / blood
  • Inflammation Mediators / metabolism
  • Male
  • Middle Aged
  • Phenotype*
  • ST Elevation Myocardial Infarction* / blood
  • ST Elevation Myocardial Infarction* / immunology
  • ST Elevation Myocardial Infarction* / pathology
  • Th1 Cells* / immunology

Substances

  • CD28 Antigens
  • Cytokines
  • Inflammation Mediators