Key result
CAD is linked to a ~15% reduction in CD16/CD56 NK cells versus healthy controls.
Why the study?
Natural killer cells may modulate inflammatory reactions contributing to adverse events in coronary artery disease, but their association with CAD and myocardial infarction forms is unclear.
Case-Control (n=190)
Effect estimate: 15% reduction
p-value: p=< 0.001
Patients with coronary artery disease exhibit significant reductions in specific natural killer cell populations and elevated inflammatory markers, highlighting the role of immune modulation in CAD.
NK cell reduction in CAD may reflect immune dysregulation; hypothesis-generating and requires prospective validation before clinical relevance.
BACKGROUND: Natural killer (NK) cells are the potential modulators of inflammatory reactions that exert several unique biological effects and could lead to future adverse events of coronary artery disease (CAD). HYPOTHESIS: The purpose of this study was to find out the possible association of modulation in NK cell, TNK cells, T cells, B cells, and tumor necrosis factor alpha (TNF-α) in CAD patients and various forms of myocardial infarction. METHODS: The present study included total 190 subjects (98 confirmed CAD patients both men and women and 92 healthy control individuals). Serum concentration of TNF-α was measured by ELISA method. For the measurement of various immune cells, viz., NK cell, TNK cells, T cells, and B cells, flow-cytometric analysis was performed. RESULTS: A significant reduction by 15% (P < 0.001) in CD16/CD56 NK cells was observed in CAD patients. Moreover, non-ST segment elevation myocardial infarction (NSTEMI), ST segment elevation myocardial infarction (STEMI), unstable angina (UA), and combined UA + NSTEMI group also showed a significant decline in NK cells compared with control individuals. CD16/CD56/CD3 TNK cells showed a significant reduction in CAD, NSTEMI, STEMI, and UA categories. However, UA + NSTEMI group did not show any significant change in TNK cells. On the other hand, the level of TNF-α was found to be significantly elevated in CAD, STEMI, and UA groups. NSTEMI and combined UA + NSTEMI group did not show any significant change in TNF-α level. CONCLUSION: Current study provides an insight toward the association of immune cells and inflammation with CAD.
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Jabir et al. (2017) conducted a case-control in Coronary Artery Disease (n=190). Coronary artery disease vs. Healthy controls was evaluated on CD16/CD56 NK cells (15% reduction, p=< 0.001). Coronary artery disease was associated with a significant 15% reduction in CD16/CD56 natural killer cells compared with healthy controls (P < 0.001).
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