Neutrophils Exhibit Delayed Spontaneous Apoptosis and Resistance to Regulatory T-Cell-Induced Apoptosis in Patients With Chronic Coronary Syndrome: Brief Report.

Authors

Maike Schneider, Camilla Skoglund, Rosanna W S Chung, Lena Jonasson

Published in

Arteriosclerosis, thrombosis, and vascular biology. Jun 25, 2026. Epub Jun 25, 2026.

Abstract

Persistent inflammation is linked to poor outcomes in patients with a history of myocardial infarction. The inflammatory state has been associated with activation of neutrophils as well as with regulatory T-cell (T_reg) deficiency. The role of T_regs in the regulation of neutrophil survival has been postulated recently. Here, we investigated neutrophil apoptosis along with the potential impact of T_regs on neutrophil apoptosis in patients with postmyocardial infarction chronic coronary syndrome, compared with healthy controls.
Twenty patients and 19 controls were included. Neutrophil apoptosis was assessed after 5-hour culture with or without IL (interleukin)-10, TNF (tumor necrosis factor), or lipopolysaccharide. Neutrophil phenotype was evaluated through flow cytometry analysis of surface receptors (CD66b and CXCR4) and ex vivo release of cytokines and proteins. The ability of T_regs to induce neutrophil apoptosis was examined in autologous neutrophil-T_reg cocultures.
Spontaneous neutrophil apoptosis was significantly delayed in patients compared with controls (10.3% versus 19.2%, P=0.025). Also, neutrophils from patients overexpressed CD66b and CXCR4 and were more prone to release proinflammatory mediators. Notably, T_regs induced neutrophil apoptosis in healthy subjects, but not in patients, indicating a loss of T_reg-mediated regulation in the latter. There was no evidence that IL-10 had any influence on neutrophil apoptosis. However, cell-to-cell contact was found essential for T_reg-induced neutrophil apoptosis.
Patients with postmyocardial infarction chronic coronary syndrome display delayed neutrophil apoptosis and a proinflammatory neutrophil phenotype that is resistant to T_reg-mediated apoptosis. Neutrophil dysfunction may contribute to persistent inflammation in patients with postmyocardial infarction chronic coronary syndrome, and as such constitutes a novel therapeutic target.

PMID:
42345095
Bibliographic data and abstract were imported from PubMed on 25 Jun 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.