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Lipid metabolism disorders form the pathological basis of AS. Immune injury resulting from lipid deposition, which is regulated by various cytokines, significantly contributes to disease progression. Follicular helper T (Tfh) cells are essential in the humoral immune response. The abnormal expression of surface molecules and cytokines by Tfh cells may contribute to the onset and progression of AS. Additionally, an increase in the Tfh cell population contributes to the progression of AS and coronary artery disease (CAD). Therefore, the targeting of Tfh cells and their associated functional molecules could serve as a promising therapeutic strategy against AS. 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