Deficit in blood MAIT cells, altered cytokines and T cell dynamics in patients with coronary artery disease

OBJECTIVES: Coronary artery disease (CAD) is a chronic inflammatory disorder characterized by immune dysregulation and a higher risk of viral infections. Among the immune cells involved, mucosal-associated invariant T (MAIT) cells participate in antimicrobial defense and tissue repair, yet their contribution to CAD has not been clearly defined. METHODS: Peripheral blood mononuclear cells and plasma were obtained from patients with CAD and from healthy controls. MAIT cell subsets, conventional T cells, and the SARS-CoV-2 receptors ACE2 and CD147 were analyzed by flow cytometry. Cytokines were quantified using ELISA. Additional in-vitro assays were performed to test whether recombinant SARS-CoV-2 spike proteins could influence cell apoptosis or proliferation. RESULTS: T cells, pointing toward an exhausted phenotype. IL-18 levels correlated negatively with left-ventricular ejection fraction. Expression of ACE2 and CD147 was similar between groups, and spike-protein exposure did not trigger significant apoptosis or proliferation in vitro. CONCLUSION: CAD is associated with loss and functional alteration of MAIT cells, cytokine imbalance, and T-cell exhaustion. Together, these immune changes may weaken antiviral defense mechanisms in the context of viral infections, such as the SARS-CoV-2 infection.