Abstract
BackgroundSerine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells.MethodsTh2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus.ResultsKnockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells.ConclusionOur results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.
Highlights
IntroductionClade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma
Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma
Knockdown of SERPINB10 expression alleviates house dust mite (HDM)‐induced airway inflammation and the T-helper type 2 (Th2) response in a murine model of asthma We wished to investigate the role of SERPINB10 in the Th2 response of allergic asthma
Summary
Clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells. Asthma is a common chronic inflammatory disease characterized by airway inflammation, airway hyperresponsiveness, mucus hyperproduction, and airway remodeling [1]. The Th2 cells and the cytokines that typify the Th2 cell subset underlies the inappropriate immune responses that characterize allergic asthma [2]. The “signature” cytokines of Th2 cells, interleukin (IL)-4, IL-5 and IL-13, have a central role in infiltration of eosinophils and increased secretion of mucus [3, 4]. Serine protease inhibitors (SERPINS) are a superfamily of homologous proteins that have important roles in inflammation, immune-system function, apoptosis. SERPINB3 and SERPINB4 in patients suffering from allergic disease control the viability of Th2 cells by exerting anti-apoptotic effects [11]
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