Allergen induced Treg response in the peripheral blood mononuclear cells (PBMCs) of patients with nasal polyposis
Authors:
- 1 January 2014
- journal article
- research article
- Published by Allergy, Asthma, and Immunology Association of Thailand in Asian Pacific Journal of Allergy and Immunology
- Vol. 32 (4) , 300-307
Abstract
Background: Nasal polyposis (NP) is a chronic inflammatory disease of the nasal cavity and sinuses regulated by T cells. Regulatory T (Treg) cells are involved in controlling immune responses and inhibiting the allergen-specific effector cell response. The aim of this study was to evaluate whether NP patients had defects in Treg cells after specific allergen exposure and the possible correlation between atopy and Treg cells. Methods: Peripheral blood mononuclear cells (PBMCs), isolated from NP patients and controls, were cultured with allergen+phytohemagglutinin (PHA) or PHA stimulation for 48h. The frequency of CD4+CD25+Foxp3+ cells was measured by flow cytometry. The level of Foxp3 was measured by Real-time PCR. Concentrations of Interferon-gamma (IFN-gamma), Interleukin-4 (IL-4), Interleukin-5 (IL-5), Interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta) in culture supernatants were determined by ELISA. Results: Both atopic and non-atopic NP patients had a significantly decreased frequency of Treg cells and Foxp3 level in allergen stimulated PBMCs, also significantly decreased TGF-beta level in culture supernatants. The decrease was even more striking in the atopic group. Also, there were significantly negative correlations between Treg cells and IFN-gamma, IL-4, IL-5. Moreover, in the atopic group, allergen stimulation downregulated Treg cells and increased IFN-gamma, IL-4, IL-5 levels, while upregulating Treg cells and decreasing IFN-gamma, IL-4, IL-5 levels in controls. Conclusions: Patients with NP have a defective Treg cell response after allergen stimulation which is related to excessive Th1 and Th2 responses to specific allergens. Atopy may increase the impairment of Treg and exacerbate NP through the defective suppression of Treg on Th1 and Th2.Keywords
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