Regulatory T-cell frequency and function in acute myocardial infarction patients and its correlation with ventricular dysfunction.
Elena Berenice Martínez-ShioLaura Sherell Marín-JáureguiAlma Celeste Rodríguez-OrtegaLesly Marsol Doníz-PadillaRoberto González-AmaroCarlos David Escobedo-UribeAdriana Elizabeth Monsiváis-UrendaPublished in: Clinical and experimental immunology (2024)
A high percentage of patients with acute coronary syndrome develop heart failure due to the ischemic event. Regulatory T (Treg) cells are lymphocytes with suppressive capacity that control the immune response and include the conventional CD4+ CD25hi Foxp3+ cells and the CD4+ CD25var CD69+ LAP+ Foxp3- IL-10+ cells. No human follow-up studies focus on Treg cells' behavior after infarction and their possible relationship with ventricular function as a sign of postischemic cardiac remodeling. This study aimed to analyze, by flow cytometry, the circulating levels of CD69+ Treg cells and CD4+ CD25hi Foxp3+ cells, their IL-10+ production as well as their function in patients with acute myocardial infarction (AMI), and its possible relation with ventricular dysfunction. We found a significant difference in the percentage of CD4+ CD25hi Foxp3+ cells and IL-10+ MFI in patients with AMI at 72 hours compared with the healthy control group, and the levels of these cells were reduced 6 months post-AMI. Regarding the suppressive function of CD4+ CD25+ regulatory cells, they were dysfunctional at 3 and 6 months post-AMI. The frequency of CD69+ Treg cells was similar between patients with AMI at 72 hours postinfarction and the control groups. Moreover, the frequency of CD69+ Treg cells at 3 and 6 months postischemic event did not vary over time. Treg cells play a role in regulating inflammation after an AMI, and its function may be compromised in this pathology. This work is the first report to evaluate CD69+ Foxp3- Treg cells in AMI patients.
Keyphrases
- induced apoptosis
- acute myocardial infarction
- cell cycle arrest
- heart failure
- immune response
- oxidative stress
- left ventricular
- chronic kidney disease
- endoplasmic reticulum stress
- end stage renal disease
- cell death
- coronary artery disease
- signaling pathway
- transcription factor
- newly diagnosed
- flow cytometry
- inflammatory response
- brain injury
- pi k akt
- acute heart failure