Allergic rhinitis (AR) is a chronic IgE-mediated inflammatory disease of the nasal mucosa that has shown a steady rise in prevalence worldwide and in Uzbekistan. The disorder arises from a breakdown of immunological tolerance caused by functional insufficiency of regulatory T cells (Tregs), leading to the dominance of Th2 and Th17 effector pathways. This review provides a comprehensive analysis of the pathophysiological mechanisms underlying AR and examines recent advances in recombinant regulatory T-cell–based immunotherapies, including chimeric antigen receptor (CAR-Treg) and B-cell antigen receptor (BAR-Treg) strategies.Through a systematic analysis of 82 publications (2010–2025), the article summarizes evidence showing reduced FOXP3⁺ Treg numbers, decreased IL-10/TGF-β levels, and elevated Th2/Th17 cytokines (IL-4, IL-5, IL-13, IL-17A) as core immunological features of AR. The findings highlight that CAR-Treg and BAR-Treg cells can re-establish antigen-specific immune tolerance by selectively targeting allergen-presenting cells and restoring mucosal homeostasis.From the perspective of Uzbekistan, where AR prevalence has increased due to air pollution, dust storms, and viral exposure, the development of recombinant T-cell–based immunotherapies represents a critical future direction for precision medicine. Integrating such cellular platforms within the national biomedical research framework could substantially improve allergy management and contribute to personalized therapeutic innovation.

Allergic rhinitis; regulatory T cells (Tregs); FOXP3; Th2/Th17 imbalance; CAR-Treg; BAR-Treg; immune tolerance; cytokines; Uzbekistan; precision immunotherapy.

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