Emerging immune networks and targeted strategies in T2 asthma

Asthma is a highly heterogeneous chronic inflammatory disease of the airways, among which Th2-high asthma represents the most prevalent endotype. The pathogenesis of Type 2 (T2) asthma (driven by type 2 inflammation) involves a complex immune network orchestrated by the coordinated actions of multiple effector cell populations, including Th2 cells, group 2 innate lymphoid cells (ILC2s), and type 2 cytotoxic T (Tc2) cells. Epithelial-derived alarmins, particularly interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP), function as key upstream initiators that bridge innate and adaptive immunity. In addition, multilayered regulatory mechanisms-including genetic susceptibility, metabolic reprogramming, and ubiquitination-collectively govern the initiation and progression of Th2-driven inflammation. With the deepening understanding of these mechanisms, therapeutic strategies have progressively shifted from targeting downstream effector molecules to upstream alarmins, thereby providing new directions for precision medicine. This review systematically summarizes recent advances in the immunopathogenesis and targeted therapies of T2 asthma, offering a conceptual framework for precision-based clinical interventions.