An Association Between GLP-1 Receptor Expression on Regulatory T Cells and the Severity of Coronary Artery Stenosis and Inflammatory Dysregulation in Coronary Heart Disease.
Level 4 - case-series / case-control
Case-control observational study
PubMed 41089793 · doi:10.31083/RCM39927
What was done
A case-control study enrolled 130 coronary heart disease (CHD) patients (stratified by Gensini score into low- and high-risk stenosis groups) and 70 non-CHD controls. Peripheral blood regulatory T cells (CD4+ CD25+ FoxP3+) and GLP-1R+ Tregs were measured using flow cytometry. Plasma levels of IL-2, IL-4, IL-6, IL-10, IL-35, and TNF-α were quantified. Associations between Treg subsets and CHD outcomes were assessed using multivariate logistic regression, ROC analysis, and Spearman correlation.
What was found
CHD patients had significantly lower proportions of total Tregs (p < 0.001) and GLP-1R+ Tregs (p = 0.013) compared with controls, with further reductions in high-risk stenosis subgroups. In multivariate logistic regression, total Tregs (CHD: OR = 0.752, p < 0.001; stenosis: OR = 0.760, p = 0.021) and GLP-1R+ Tregs (CHD: OR = 0.859, p = 0.013; stenosis: OR = 0.840, p = 0.040) independently predicted disease and stenosis severity. Diagnostic accuracy was modest for total Tregs (CHD: AUC = 0.663; stenosis: AUC = 0.635) and GLP-1R+ Tregs (CHD: AUC = 0.600; stenosis: AUC = 0.619). GLP-1R+ Treg proportion correlated weakly with IL-35 (r = 0.185, p = 0.016) and inversely with IL-4 (r = -0.150, p = 0.047).
Why it matters
This study links reduced GLP-1 receptor expression on regulatory T cells to coronary heart disease and stenosis severity, highlighting a potential immunomodulatory pathway in atherogenesis.
Limits
The case-control design prevents determination of causality. The sample size is modest (n = 200). Diagnostic discrimination is relatively weak (AUCs 0.600–0.663) and cytokine correlations are minimal (|r| < 0.20). Crucial clinical confounders such as diabetes status, statin use, and baseline metabolic medications were not reported in the abstract.
Cited by
- supports GLP-1 binds directly to receptors on immune cells.