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Immune system modulation via repeated exposure to allergen" refers to the process underlying **allergen-specific immunotherapy** or **desensitization**, where controlled and repeated administration of an allergen leads to changes in the immune response. This is not a single molecular entity but rather describes an overall therapeutic approach that aims to induce immune tolerance. The mechanism involves several key steps: • Initial sensitization occurs when antigen-presenting cells present allergens on MHCII molecules to T cells. This leads to differentiation into Th2 helper cells under the influence of interleukins such as IL‑4. Th2 cells then stimulate B cell-derived plasma cells to produce IgE antibodies specific for the allergen. • Upon re-exposure, these IgE antibodies bind high-affinity FcεRI receptors on mast cells and basophils. Crosslinking triggers degranulation and release of inflammatory mediators like histamine, prostaglandins, leukotrienes, causing allergic symptoms[1][3]. • Repeated controlled exposure through immunotherapy can shift this response toward increased regulatory T cell activity—especially Foxp3+ Tregs—which suppress effector T cell responses through secretion of anti-inflammatory cytokines such as IL‑10 and TGF‑β[2]. This reduces Th2-driven inflammation and promotes long-term tolerance. • The process also involves changes in antibody class switching from IgE toward non-inflammatory isotypes like IgG4. This concept does not refer to any one protein/receptor/enzyme/transporter but rather encompasses multiple cellular pathways involved in allergy development and resolution. Therefore it should not be considered a canonical therapeutic target at the molecular level. If you require structured information about individual molecules involved—such as FcεRI receptor or regulatory T cell markers—please specify those targets individually.
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