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"Immune system modulation via repeated allergen exposure" refers to the process by which the immune response is altered or recalibrated through frequent, controlled exposure to a specific allergen. This principle underlies allergen-specific immunotherapy (AIT), a treatment for allergic diseases. During AIT, repeated low-dose allergen administration leads to changes such as desensitization of mast cells and basophils, increased production of regulatory cytokines (IL-10, TGF-β), induction of regulatory T cells (Tregs), and a shift from pathogenic Th2 responses (characterized by IL-4, IL-5, and IgE production) to more tolerogenic or balanced immune responses. Biological mediators and pathways involved in this process include T cell subsets (particularly Tregs and Th2 cells), dendritic cells, B cells, IgG4 antibodies, and cytokines such as IL-4, IL-5, IL-10, and TGF-β. Molecular pathways like the NF-κB and Hippo signaling pathways—as well as Notch signaling—play critical roles in immune cell differentiation and tolerance[1][2][3][4][5]. Biologic drugs and allergen extracts used in immunotherapy target these mechanisms but no single molecule or receptor embodies the entire process. In summary, "Immune system modulation via repeated allergen exposure" is a **therapeutic process** or strategy and not a molecular target; relevant molecular targets in this process include cytokine receptors (e.g., IL-4R, TSLP receptor, IgE receptor), T cell subsets, and signaling pathways.
Induction of regulatory T cell (Treg) activity; Suppression of effector Th2 responses; Promotion of blocking antibodies (IgG4); Inhibition of IgE-mediated mast cell and basophil activation
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