Abstract
Enhancer of zeste homolog 2 (Ezh2) has been shown to play a role in the differentiation of T helper (Th) 1 and 2 cells in mice studies using Ezh2-deficient T cells. However, the results have been inconsistent, and the function of Ezh2 in human Th1 and Th2 cell differentiation and its association with disease remains controversial. We measured the expression of Ezh2 in Th1 and Th2 cells in peripheral blood mononuclear cells after acute challenge with house dust mite using flow cytometry in patients with allergic rhinitis (AR) and controls. The role of Ezh2 was further explored by adding the p38 inhibitor to see if this affected allergen-induced Th1 and Th2 differentiation. The expression of Ezh2 in the Th1 and Th2 cells was significantly lower in the patients than in the controls and was negatively correlated with serum IL-17A levels in the patients. Ex vivo allergen challenge resulted in rapid Th2 cell differentiation, which was negatively associated with the Ezh2 expression in Th2 cells. Inhibiting p38 activity increased the expression of Ezh2 in Th2 cells and reduced the number of differentiated Th2 cells. Our findings suggest that Ezh2 expression is potentially associated with AR development.
Highlights
Allergic rhinitis (AR) is very common worldwide and impacts the ability to work, performance at school, sleep, and quality of life
We evaluated the percentages of Th1 and Th2 cells in the CD4+ T cells, and the expression of Enhancer of zeste homolog 2 (Ezh2) in the Th1 and Th2 cells compared to the naïve T cells
There were no significant differences between the two groups in any of the examined variables, the control group was slightly older than the allergic patients
Summary
Allergic rhinitis (AR) is very common worldwide and impacts the ability to work, performance at school, sleep, and quality of life. T helper (Th) 2 cells are known to play a prominent role in allergic inflammation initiated by an immunological response to allergens such as dust mites. Th2 cells secrete cytokines such as interleukin-4 (IL-4) to induce B cell isotype switching and immunoglobulin E (IgE) secretion [1]. Various immune mechanisms counterbalance IgE-mediated processes, of which IL-10 has attracted the most attention [1]. Antigen-activated naive CD4+ T cells can give rise to Th effector subsets that are tailored to their respective roles by secreting specific cytokines. While a growing body of evidence has indicated the complexity of immunological processes in AR, the role of Th2 cells and consequent IgE responses remain at the forefront of current research.
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