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Allergen-specific immune cells represent a heterogeneous population of leukocytes, primarily Th2-polarized T cells and IgE-secreting B cells, that mediate hypersensitivity to normally harmless environmental substances (Akdis, M., & Akdis, C. A., 2014, J Allergy Clin Immunol). These cells are central to the pathophysiology of allergic diseases, where they orchestrate the production of allergen-specific IgE and the subsequent activation of mast cells and basophils (Galli, S. J., et al., 2008, Nature). Therapeutic interventions often focus on modifying the activity of these cells, such as Allergen Immunotherapy (AIT), which promotes the development of regulatory T (Treg) and B (Breg) cells to induce long-term clinical tolerance (Shamji, M. H., & Durham, S. R., 2017, J Allergy Clin Immunol). Emerging precision therapies, including CAR-T cells and monoclonal antibodies like Omalizumab, target the specific receptors or products of these cells to prevent allergic cascades (Ward, S. T., et al., 2022, Front Immunol). Monitoring these cell populations through biomarkers like specific IgE/IgG4 ratios and cytokine profiles is essential for assessing treatment efficacy and patient selection (Larche, M., et al., 2006, Nat Rev Immunol).
The primary mechanism involves the induction of peripheral T-cell tolerance, characterized by a shift from a Th2-dominated response to a Th1 or regulatory T cell (Treg) dominated response, leading to reduced IL-4, IL-5, and IL-13 production (Akdis, C. A., 2012, Nat Rev Drug Discov). This is often accompanied by the production of blocking antibodies such as IgG4, which compete with IgE for allergen binding, and the suppression of allergen-specific IgE production by B cells (Shamji, M. H., et al., 2011, J Allergy Clin Immunol).
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