Abstract
Hashimoto's thyroiditis is one of the most common autoimmune diseases, characterized by lymphocytic infiltration, thyroid autoantibody production, and progressive thyroid destruction. Natural killer cells, as innate immune effectors, play a dual role in HT pathogenesis through cytotoxicity, death receptor signaling, inflammasome activation, and secretion of proinflammatory cytokines. Recent studies using single-cell RNA sequencing have revealed functional heterogeneity of NK subsets, suggesting stage-specific roles in either amplifying or regulating inflammation. Moreover, peripheral blood from HT patients shows increased expression of activating receptors such as NKG2D and NKp30, positively correlated with thyroid autoantibody titers, while abnormal activation of the NLRP3 inflammasome drives NK cell-mediated IFN-γ release and thyroid follicular cell pyroptosis. These advances highlight NK cells as both contributors to immune imbalance and potential therapeutic targets. A better understanding of NK cell-related mechanisms will provide novel insights into disease monitoring and the development of targeted interventions for HT.