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Immune system desensitization via controlled exposure to specific food allergens—commonly known as allergen immunotherapy—refers to a clinical approach in which patients are repeatedly exposed to gradually increasing doses of the offending food protein, such as peanut or cow’s milk protein, in order to induce a state of immunological tolerance. This process is mediated through shifts in antibody class (reduction of allergen-specific IgE and elevation of IgG4), expansion of allergen-specific regulatory T cells, and suppression of effector cells like mast cells and basophils that drive allergic responses. Such immunotherapy is used experimentally and increasingly in clinical practice to treat food allergies, though it is not attributable to a single molecular target but comprises a coordinated alteration of immune responses at the cellular and molecular levels[1][2][3][4].
Induction of allergen-specific regulatory T cells (Tregs) that secrete IL-10 and TGF-beta, promoting immune tolerance. Suppression of mast cells and basophils to increase threshold for anaphylaxis. Shift in antibody profile: decrease in antigen-specific IgE and increase in IgG4 ("blocking" antibodies). Downregulation of effector Th2 cell responses, often through a Th2-to-Th1 and regulatory shift.
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