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Isolation and Identification of Extravascular Immune Cells of the Heart
Published on: August 23, 2018
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Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation
Fernanda Bocanegra-Zamora1, Fernanda Espinosa-Bautista1,2, Gian M Jiménez-Rodríguez3
1Immunology Department, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Journal of Vascular Research
|September 18, 2024
Summary
In ST-elevation myocardial infarction (STEMI), senescent CD4+CD28null cells are increased and predominantly exhibit a Th1 phenotype. These cells are equally distributed in the coronary circulation of STEMI patients.
Area of Science:
- Immunology
- Cardiology
- Cell Biology
Background:
- Inflammation plays a key role in ST-elevation myocardial infarction (STEMI).
- Early senescent CD4+CD28null cells are implicated in STEMI pathogenesis.
- The functional phenotype of these cells in the coronary circulation is not well understood.
Purpose of the Study:
- To investigate the functional phenotype of CD4+CD28null cells in the coronary circulation of STEMI patients.
- To compare CD4+ cell subpopulations between STEMI patients and healthy controls.
Main Methods:
- Blood samples were collected from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of 7 healthy controls.
- Flow cytometry was used to analyze CD4+ cell subpopulations, including CD4+CD28null cells.
- Cytokine levels were measured in different vascular compartments.
Main Results:
- STEMI patients had reduced CD4+ cell counts compared to controls.
- The proportion of CD4+CD28null cells was significantly higher in STEMI patients (20.1%) versus controls (6.1%).
- In STEMI patients, CD4+CD28null cells predominantly displayed a Th1 phenotype (47.8% vs. 6.6% in controls). No significant differences in CD4+CD28null cells or cytokine levels were found between the coronary sinus and vena cava.
Conclusions:
- CD4+CD28null cells are elevated in STEMI and primarily adopt a Th1 phenotype.
- These cells are uniformly distributed within the coronary circulation in STEMI patients.
- The findings provide insights into the role of specific immune cell subsets in STEMI pathophysiology.

