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Published on: August 9, 2024
Loss of Regulatory Immune Function in Coronary Artery Disease Patients from the Indian Population
Thiruvelselvan Ponnusamy1, Srikanth Komarulu Venkatachala2, Manjunatha Ramanujappa3
1Research Scholar at Manipal University, Molecular Immunology Unit, Thrombosis Research Institute, Bangalore, India.
Insights
Inflammatory T cells and monocytes increase with coronary artery disease severity. These cells, particularly Th17 cells, show heightened responses and impaired regulation, contributing to disease progression and recurrent cardiac events.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Pathophysiology
Background:
- The role of specific inflammatory immune cells in coronary artery disease (CAD) manifestations remains unclear.
- Understanding immune cell subsets in different CAD presentations is crucial for targeted therapies.
Purpose of the Study:
- To investigate the frequency and function of inflammatory T cell and monocyte subsets in various CAD manifestations.
- To correlate immune cell profiles with clinical outcomes, including recurrent cardiac events and clinical improvement.
Main Methods:
- Flow cytometry analysis of T cell (Th17, Treg) and monocyte subsets in 181 CAD patients (stable angina, NSTEMI, STEMI, unstable angina) and 34 controls.
- Assessment of cellular responses to autoantigens (HSP60), regulatory cell function, foam cell formation, and macrophage differentiation.
- Longitudinal sample collection during cardiac events and clinical improvement.
Main Results:
- A stepwise increase in Th17 cells and monocytes was observed across the spectrum from stable angina to unstable angina.
- Higher proportions of inflammatory cells correlated positively with recurrent cardiac events and inversely with clinical improvement.
- CAD patients exhibited Th17 cell expansion in response to autoantigen HSP60 and impaired regulatory T cell (Treg) function.
Conclusions:
- Stress-induced activation of inflammatory cells, specifically Th17 cells and monocytes, is implicated in CAD progression.
- Compromised Treg function exacerbates the inflammatory response in CAD patients.
- Immune cell profiling offers potential biomarkers for CAD severity and prognosis.
Abstract:
The pathogenic roles of inflammatory T cells and monocytes subsets have not been explored in different manifestations of coronary artery disease. We studied the frequency of these cells, their response to autoantigens, regulatory cell functional assay, foam cell formation and macrophage differentiation in 181 patients (stable angina, ST-elevated myocardial infarction (STEMI), NSTEMI, and unstable angina), and 34 controls and in samples collected during recurrent cardiac events and from patients showing clinical improvement. The proportion of Th17 cells and monocytes gradually increased in patients with stable angina at one end of the spectrum followed by NSTEMI, STEMI, and unstable angina at other end. Inflammatory cells were positively and inversely associated with recurrent events and clinical improvement, respectively. Patients showed expansion of Th17 cells in response to autoantigen (HSP60) and compromised Treg function. Our results suggest that stress-induced activation of inflammatory cells expands in the absence of regulatory control in CAD patients.
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