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Allergic rhinitis (AR) is the inflammation of nasal mucosa due to the type 1 hypersensitivity reactions mediated by immunoglobulin E (IgE) and triggered by certain allergens. The latest concept in allergic disease is the role of regulatory T cells (Treg). Interleukin-2 enhances the function and survival of Treg to perform its function as a controller of effector for forming a tolerant system by suppressing and regulating the homeostasis system. Treg has a transcription factor FoxP3 which plays a role in developing major function of Treg and progression to produce IL-10 and TGF-s. The atopic diseases are caused by a deficiency of Treg. The new perspective is low-dose IL-2 therapy towards autoimmune disease and allergic inflammation. Low-dose IL-2 therapy requires further clinical studies to optimize the dose, time, and the schedule of the IL-2 treatment. FoxP3 has the potential to assist in evaluating the active process of immunological process, which cannot be evaluated by Th1 and Th2 markers, and FoxP3 can be a successful immunotherapy marker.

The Role of Cytokine Interleukin-2, Transcription Factor of FoxP3 in the Immunological Regulation of Allergic Rhinitis