Allergen-specific immune axis

The allergen-specific immune axis, primarily represented by the T helper 2 (Th2) or Type 2 immune pathway, is a coordinated biological system responsible for the development and execution of allergic responses (Int. J. Biol. Sci., 2026; PMC, 2024). This axis is triggered when allergens are recognized by the immune system, leading to the differentiation of Th2 cells and the activation of type 2 innate lymphoid cells (ILC2s) (Int. J. Biol. Sci., 2026). These cells release a signature profile of cytokines, including interleukin-4 (IL-4), IL-5, and IL-13, which drive the production of allergen-specific IgE, eosinophil recruitment, and tissue remodeling (PMC, 2024; Int. J. Biol. Sci., 2026). IgE antibodies bind to high-affinity receptors (FcεRI) on mast cells and basophils, sensitizing them to subsequent allergen exposure, which triggers the release of histamine and other inflammatory mediators (MDPI, 2024). Therapeutic strategies targeting this axis include monoclonal antibodies that neutralize IgE (e.g., omalizumab) or specific cytokines and their receptors (e.g., dupilumab, mepolizumab), effectively dampening the allergic cascade in conditions like asthma, atopic dermatitis, and allergic rhinitis (Frontiers, 2024; Int. J. Biol. Sci., 2026). While highly effective, modulating this axis can lead to safety concerns such as an increased susceptibility to helminth infections and specific side effects like conjunctivitis or injection site reactions (Helda, 2025).

Other names

Th2 immune axisType 2 immune axisAllergic cascadeIgE-mediated immune pathwayTh2 pathwayType 2 inflammation

Targeted inhibition of key molecular components within the Th2/Type 2 pathway, including IgE, IL-4, IL-5, IL-13, and TSLP, to suppress the allergic inflammatory cascade.