is an International, peer-reviewed scientific journal that publishes original article in experimental & clinical medicine and related disciplines such as molecular biology, biochemistry, genetics, biophysics, bio-and medical technology. JMS is issued four times per year on paper and in electronic format.

Background: A new concept in understanding allergic diseases is regulatory T cells (Tregs), which control the immune reaction caused by Th2 cytokine production. Forkhead Box Protein 3 (FoxP3) is a marker that has a critical role in the development and function of Tregs. Some studies found differences in FoxP3 level and in Tregs capacity to control immune reactions in allergic diseases. The aim of this study was to investigate FoxP3 level in Allergic rhinitis (AR) patients compared to atopic and healthy/normal persons in Jakarta. Methodology: This study used observation to analyze the level of FoxP3 in AR, atopic and healthy/normal persons, and used ELISA to measure the FoxP3 level. Results: The study had sixty participants divided into three groups: 21 in the Normal group, 16 in the Atopic group, and 23 in the AR group. The mean FoxP3 levels were 0.81 ± 0.35 in the normal group, 3.42 ± 0.15 in the atopic group, and 3.40 ± 0.13 in the AR group. Statistical analysis with Mann-Whitney tests indicated significant differences, with AR and atopic groups having higher FoxP3 levels than the normal group, (p = 0.001), and no statistically significant differences between the AR and atopic groups, (p = 0.92). Conclusion: Our study results suggested that FoxP3 was active in the control of inflammatory processes due to allergies, and decrease level of FoxP3 indicated severe AR, but suggested another mechanism caused differences in the clinical phenotypes of AR and atopic patients, despite them having equally high levels of FoxP3.

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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-β. 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.

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