Background: T regulatory cell (Treg) plays a critical role in respiratory allergy and allergen-specific immunotherapy (SIT), and γδ T cells might participate in mediating Treg quantity and/or function in some immunological diseases. To further characterize whether γδ T cells could influence Treg in allergic rhinitis (AR) and SIT, we investigated the expression pattern of Treg's Foxp3 gene and γδ T cell receptor (TCR) Vγ subfamily genes in peripheral blood mononuclear cells (PBMCs) of AR patients before and after SIT.
Methods: Eighteen AR patients undergoing effective SIT with house dust mite extract for one year were recruited. Visual Analogue Scale (VAS) was applied to evaluate the severity. Immunofluorescence quantification analysis was performed to determine the serum specific IgE (sIgE) content. Real-time PCR was used to detect the expression levels of Foxp3 and TCR Vγ subfamilies. Ten healthy volunteers were recruited as the controls.
Results: Nasal uni-VAS score after SIT was significantly lower than that before SIT, while serum sIgE content was similar before and after SIT. Expression levels of Foxp3 and TCR Vγ subfamilies in AR patients before treatment were significantly lower than those in healthy subjects. Expression levels of VγI and II were similar before and after SIT, while expression levels of Foxp3 and VγIII after SIT were significantly higher than those before. Before SIT, the significant positive correlation was observed between expression levels of Foxp3 and VγI, II, III, while negative correlation was observed between Foxp3, VγIII and VAS. After SIT, the significant positive correlation between expression levels of Foxp3 and VγIII and negative correlation between Foxp3, VγIII and VAS were observed.
Conclusions: Treg and Vγ subfamily T cells were in a dynamic equilibrium in AR patients before and after effective immunotherapy for one year. The early improvement of symptoms following immunotherapy might be independent of the serum sIgE content in AR patients, but associated with the reconstitution of T cell immunity.