Abstract

Background: The involvement of CD4+CD25+ regulatory T cells (CD4+CD25+ TRegs) in allergic diseases was reported previously. However, it remains unclear whether CD4+CD25+ TRegs are involved in allergic rhinitis (AR). Methods: Fresh whole blood from 20 patients with AR and 16 healthy donors was used to investigate the frequency of CD4+CD25+ and CD4+CD25hi Treg cells using flow cytometry. In addition, serum total IgE (IU/mL) levels were determined using enzyme-linked immunosorbent assays. Results: Patients with AR had fewer CD4+CD25+ Treg cells (2.80 ± 1.36% vs. 3.94 ± 0.97%, P < 0.01) and CD4+CD25hi TRegs (1.53 ± 0·62% vs. 2.00 ± 0.52%, P < 0.05) than control subjects. The number of CD4+CD25+ and CD4+CD25hi TRegs was correlated negatively with total immunoglobulin E levels (r = –0.79, P < 0.01 and r = –0.61, P < 0.01, respectively). Conclusion: Deficient regulatory T cells might play a role in the development of AR.

Highlights

  • Allergic rhinitis (AR) is an example of a persistent inflammatory disease of the nasal mucosa

  • The activation of Th2 cells is thought to play an important role in allergic reactions by mediating immunoglobulin E (IgE) synthesis and eosinophilic inflammation via IL-4, IL-5, and IL-13 [16, Figure 2

  • Allergen-induced T cell proliferation can be detected in primary cultures of peripheral blood mononuclear cells (PBMCs) from individuals both with and without allergies

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Summary

Introduction

Allergic rhinitis (AR) is an example of a persistent inflammatory disease of the nasal mucosa. It is caused by the secretion of interleukin (IL)-4, IL-5, and IL-13 by CD4+ Th2 effector cells in response to harmless environmental antigens [1]. The T cells that infiltrate the nasal mucosa are predominantly Th2 in nature, and they release cytokines that promote immunoglobulin E (IgE) production by plasma cells. The involvement of CD4+CD25+ regulatory T cells (CD4+CD25+ TRegs) in allergic diseases was reported previously. It remains unclear whether CD4+CD25+ TRegs are involved in allergic rhinitis (AR). Conclusion: Deficient regulatory T cells might play a role in the development of AR

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