Abstract
Atrial fibrillation (AF) is a common arrhythmia associated with severe outcomes like heart failure and stroke. Recent studies highlight the crucial role of T in AF. Clinical studies have observed elevated levels of CD4(+)CD28(null) T cells, Th17/Treg cells, CD8(+) cells, and related markers in the peripheral blood or atrial tissue of AF patients, correlating with disease severity and cardiovascular events. These T cell subsets contribute to AF through: (1) releasing inflammatory factors like TNF-α and IL-17 which affect calcium homeostasis and electrical activity in atrial myocytes and/or promote atrial fibrosis; (2) recruiting inflammatory cells such as macrophages, causing local inflammation, oxidative stress, and atrial remodeling; (3) secreting cytotoxic proteins like perforin and granzymes, inducing apoptosis in atrial myocytes and affecting their action potentials; (4) direct contact, influencing atrial myocyte electrophysiology. Understanding these T cell-mediated mechanisms may uncover new therapeutic targets for AF.