Pulmonary hypertension (PH) is a complex and progressive syndrome characterized by vascular remodeling, inflammation, and immune imbalance. Although T cell dysregulation is increasingly recognized in PH, their precise role remains controversial. Pathogenic subsets, such as T helper 17 cells (Th17), promote vascular inflammation and smooth muscle proliferation through cytokines including IL-17 and IFN-γ, whereas regulatory T cells (Tregs) counteract these processes by suppressing excessive immune responses and maintaining endothelial stability. In PH, T cell homeostasis is largely shaped by signals from macrophages, dendritic cells, vascular cells and so on. Yet they are not bystanders: once activated, T cells engage in cytokine release and intercellular interactions. Importantly, their activation may represent a secondary consequence of disease, a primary trigger of vascular injury, or a protective mechanism depending on the context. This review integrates current evidence to describe the multifaceted roles of T cells in PH, evaluate their therapeutic potential, and clarify their diverse functions as pathogenic amplifiers or protective regulators in disease progression.