Table 1.

Role of Th2 Cells and Their Key Cytokines in Allergic Rhinitis

Immune Component	Main Function	Key Mechanisms	Reference
Th2 Cell	Core of the type 2 immune response; initiates the allergic cascade.	Allergens presented by APCs to naive CD4+ T cells, which differentiate into Th2 cells under cytokines like IL-4; Differentiation is dominated by the key transcription factor GATA3, regulated by the IL-4/JAK/STAT6 signaling pathway; Increased number of Th2 cells in AR patients leads to a Th1/Th2 imbalance skewed towards Th2.	1-3, 21
IL-4	Drives Th2 cell differentiation and induces B cells to produce allergen-specific IgE antibodies.	Drives naive T cell differentiation towards Th2 phenotype by activating the STAT6 signaling pathway and upregulating GATA-3; Directly induces immunoglobulin class switching in B cells to produce IgE; Type 2 T follicular helper (Tfh2) cells are a major source of IL-4, inducing memory B cells to express CD23; Blocking IL-4 or depleting CD4+ T cells inhibits serum IgE production.	6-8, 10, 11
IL-5	Recruits and activates eosinophils, leading to the late-phase reaction and chronic inflammation.	In Nasal Allergen Challenge (NAC) models, elevated IL-5 levels drive eosinophil migration from blood to nasal mucosa; Directly activates eosinophils - anti-IL-5 antibody can inhibit this activation; Persistent activation of the IL-5/eosinophil axis is key to AR transitioning to chronic inflammation; Pharmacological reduction of IL-5 levels significantly reduces eosinophil infiltration and improves clinical symptoms.	12-17
IL-13	Causes mucus hypersecretion and tissue remodeling.	Directly stimulates airway epithelial cells to produce and secrete mucus, particularly MUC5AC; Promotes goblet cell hyperplasia, increasing mucus secretion sources; Acts primarily by activating the STAT6 signaling pathway; Collaborates with eosinophil recruitment and subepithelial fibrosis in IL-13-mediated airway tissue remodeling.	18-22, 24, 26