{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T06:47:35Z","timestamp":1785912455105,"version":"3.56.0"},"reference-count":55,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"vor","delay-in-days":215,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>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\u2010lymphocyte subsets and immunomodulatory drug targets influenced AF risk.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p>\n                      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 (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). A subsequent two\u2010sample Mendelian randomization (MR) analysis, which assessed 731 immune traits and included drug\u2010target MR, established causal relationships. It showed that increased counts of CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD8dim T cells (OR\u2009=\u20091.03,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002) and IgD\n                      <jats:sup>\u2212<\/jats:sup>\n                      CD38dim B cells (OR\u2009=\u20091.06,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0003) elevated AF risk. Furthermore, IL\u20106R\u2010mediated CRP elevation increased AF risk (OR\u2009=\u20091.33,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20095.18E\u20107), whereas higher IL\u201018 gene expression was protective (OR\u2009=\u20090.95,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.036).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Immune dysfunction, especially T lymphocyte subsets, is a risk factor for the development of AF. The IL\u20106R signaling pathway may be a potential target for AF prevention, whereas the use of IL\u201018 inhibitors may increase the risk of AF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/cdr\/4440768","type":"journal-article","created":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T06:03:31Z","timestamp":1785909811000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Analysis of the Correlation Between Helper T\u2010Lymphocyte Subsets and Atrial Fibrillation: An Observational and Mendelian Randomization 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