Background: Allergic rhinitis (AR) is a Th2 predominant disease, and its pathogenic mechanism is still poorly understood. CD4(+)CD25(+) T cells account for approximately 5% to 10% peripheral CD4(+) T cells and has been shown to regulate the activation of effector T cells in the periphery. The activity of CD4(+)CD25(+) T cells is associated with the transcription factor Foxp3. The present study aimed to evaluate the possible role of CD4(+)CD25(+) T cells as well as Foxp3 in the pathogenesis of AR.
Methods: Nasal tissues and peripheral blood mononuclear cells (PBMCs) were obtained from 17 patients with AR and 11 control subjects. Foxp3 was detected in nasal tissues by immunohistochemistry and real-time reverse transcription-polymerase chain reaction (RT-PCR). CD4(+)CD25(+) T cells and Foxp3 were evaluated in PBMCs by using flow cytometry. Concentrations of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) were measured by enzyme-linked immunosorbent assay (ELISA) in cultured PBMCs in the presence or absence of stimulation with phorbol ester (PMA) and Ionomycin.
Results: The numbers of Foxp3(+) cells was 129.5 +/- 35.6 and 44.2 +/- 20.5 cells/mm(2) in nasal mucosa of two groups (P < .05). There were less Foxp3(+) lymphocytes and decreased Foxp3 mRNA in AR compared with the control (P < .05). The frequencies of the CD4(+)CD25(+) population in PBMCs of two groups were 1.99 +/- 0.95% and 3.55 +/- 1.27% (P < .05). There was significant difference in the frequencies of the Foxp3(+)CD4(+) CD25(+) population (1.81 +/- 0.77 vs 3.37 +/- 1.04, P < .05) and mean fluorescence intensity (MFI) of Foxp3 (5.93 +/- 2.64 vs 11.72 +/- 4.29, P < .05) in PBMCs of two groups. After stimulation, the concentrations of IL-2 and IFN-gamma were 182.72 +/- 85.11 pg/mL and 348.94 +/- 151.88 pg/mL in PBMCs with AR, while those were 90.6 +/- 61.5 pg/mL and 155.64 +/- 68.33 pg/mL in controls (P < .05).
Conclusion: Our results indicate that CD4(+) CD25(+) regulatory T cells as well as Foxp3 may play a crucial role in immunological imbalance of AR. These findings suggest that increasing Foxp3 and CD4(+)CD25(+) T cells have the potential to be new therapeutic targets for the treatment of AR.