Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study.
J, L., Y, Y., H, F., Z, H., Y, Y., R, B., X, W., & B, L. (2026). Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study.. Cardiovascular therapeutics. https://doi.org/10.1155/cdr/4440768
J L, Y Y, H F, Z H, Y Y, R B, et al. Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study.. Cardiovascular therapeutics. 2026; doi: 10.1155/cdr/4440768
J L, Y Y, H F, et al. Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study.[J]. Cardiovascular therapeutics. 2026. DOI: 10.1155/cdr/4440768.
@article{j2026,
author = {Li J and Yang Y and Fan H and Huang Z and Yuan Y and Bai R and Wang X and Liang B},
title = {Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study.},
journal = {Cardiovascular therapeutics},
year = {2026},
doi = {10.1155/cdr/4440768},
note = {PMID: 42552764},
}
TY - JOUR AU - Li J AU - Yang Y AU - Fan H AU - Huang Z AU - Yuan Y AU - Bai R AU - Wang X AU - Liang B TI - Analysis of the Correlation Between Helper T-Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization Study. T2 - Cardiovascular therapeutics PY - 2026 DO - 10.1155/cdr/4440768 AN - PMID:42552764 ER -
BACKGROUND: Atrial fibrillation (AF) is the predominant arrhythmia. Growing evidence indicates that immunological diseases may play a role in its development. This study combined observational and genetic analyses to investigate how T-lymphocyte subsets and immunomodulatory drug targets influenced AF risk. METHODS AND RESULTS: This study retrospectively analyzed T lymphocyte subsets in 302 AF patients and 183 healthy controls. After balancing covariates via 1:1 propensity score matching, multivariate regression revealed AF patients had significantly higher absolute counts of Th1 and Th17 cells, and higher Th1/Th2 and Th17/Treg ratios (p < 0.05). A subsequent two-sample Mendelian randomization (MR) analysis, which assessed 731 immune traits and included drug-target MR, established causal relationships. It showed that increased counts of CD4+CD8dim T cells (OR = 1.03, p = 0.002) and IgD-CD38dim B cells (OR = 1.06, p = 0.0003) elevated AF risk. Furthermore, IL-6R-mediated CRP elevation increased AF risk (OR = 1.33, p = 5.18E-7), whereas higher IL-18 gene expression was protective (OR = 0.95, p = 0.036). CONCLUSION: Immune dysfunction, especially T lymphocyte subsets, is a risk factor for the development of AF. The IL-6R signaling pathway may be a potential target for AF prevention, whereas the use of IL-18 inhibitors may increase the risk of AF.