Cellular immunology · 2026
Deficit in blood MAIT cells, altered cytokines and T cell dynamics in patients with coronary artery disease.
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Stavridis Dimitrios, Wacker Max, Safarov Rauf, Testa Nicola, Awad George, Varghese Sam, Borucki Katrin, Wippermann Jens, Veluswamy Priya
Аннотация
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: The number of circulating MAIT cells was markedly reduced in CAD, most notably within the CD8+ population. In contrast, CD4+ MAIT cells were relatively increased but expressed less CCR5 intensities, suggesting limited migratory ability. Plasma IL-7 concentrations were lower in CAD, while IL-18 and IFN-α2 were higher. These findings indicate a disturbed cytokine environment, especially for MAIT cell activation. CAD samples also showed more CD4+PD-1+ and fewer CD8+CD69+ 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.
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: The number of circulating MAIT cells was markedly reduced in CAD, most notably within the CD8+ population. In contrast, CD4+ MAIT cells were relatively increased but expressed less CCR5 intensities, suggesting limited migratory ability. Plasma IL-7 concentrations were lower in CAD, while IL-18 and IFN-α2 were higher. These findings indicate a disturbed cytokine environment, especially for MAIT cell activation. CAD samples also showed more CD4+PD-1+ and fewer CD8+CD69+ 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.