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. Here, IL17A is linked to atrial fibrillation.