دورية أكاديمية

Human eosinophils release IL-1ß and increase expression of IL-17A in activated CD4+ T lymphocytes.

التفاصيل البيبلوغرافية
العنوان: Human eosinophils release IL-1ß and increase expression of IL-17A in activated CD4+ T lymphocytes.
المؤلفون: Esnault, S.1, Kelly, E. A. B.1, Nettenstrom, L. M.2, Cook, E. B.1, Seroogy, C. M.2, Jarjour, N. N.1
المصدر: Clinical & Experimental Allergy. Dec2012, Vol. 42 Issue 12, p1756-1764. 9p. 1 Chart, 5 Graphs.
مصطلحات موضوعية: *EOSINOPHILS, *INTERLEUKINS, *T cells, *RESPIRATORY allergy, *IMMUNOREGULATION
مستخلص: Background Differentiation and activation of CD4+ T cells is controlled by various cytokines produced by innate immune cells. We have shown that eosinophils ( EOS) have the potential to influence Th1 and Th2 cytokine generation by CD4+ cells, but their influence on IL-17A ( IL-17) has not been established. Objective The purpose of this study is to determine the effect of EOS on IL-17 production by lymphocytes. Methods Pre-activated CD4+ T cells were cultured in the presence of either autologous EOS or EOS culture supernatants. Expression of IL-17 was determined by real-time quantitative PCR ( qPCR) after 5 h and protein level was measured after 48 h. To determine the effect of allergen-induced airway EOS on IL-17, subjects with mild allergic asthma underwent bronchoscopic segmental bronchoprovocation with allergen (SBP-Ag) after a treatment with an anti-IL-5 neutralizing antibody (mepolizumab) to reduce airway eosinophilia. IL-17 mRNA was measured in bronchoalveolar lavage (BAL) cells by qPCR. Results In vitro, EOS significantly increased IL-17 production by CD4+ T cells. Addition of exogenous IL-1ß increased expression of IL-17 mRNA by CD4+ T cells. EOS expressed and released IL-1ß. Furthermore, levels of IL-1ß in EOS supernatants highly correlated with their ability to increase IL-17 expression by CD4+ T cells, and neutralizing antibody to IL-1ß reduced expression of IL-17 mRNA. In vivo, reduction of EOS in the airway using mepolizumab was associated with diminished IL-17 expression after SBP-Ag. Conclusions and clinical relevance Our data demonstrate that EOS can promote IL-17 production through the release of IL-1ß. Enhanced IL-17 cytokine production is another mechanism by which EOS may participate in pathogenesis of allergic airway inflammation in asthma. [ABSTRACT FROM AUTHOR]
قاعدة البيانات: Academic Search Index
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Array ( [Name] => Abstract [Label] => Abstract [Group] => Ab [Data] => Background Differentiation and activation of CD4+ T cells is controlled by various cytokines produced by innate immune cells. We have shown that eosinophils ( EOS) have the potential to influence Th1 and Th2 cytokine generation by CD4+ cells, but their influence on IL-17A ( IL-17) has not been established. Objective The purpose of this study is to determine the effect of EOS on IL-17 production by lymphocytes. Methods Pre-activated CD4+ T cells were cultured in the presence of either autologous EOS or EOS culture supernatants. Expression of IL-17 was determined by real-time quantitative PCR ( qPCR) after 5 h and protein level was measured after 48 h. To determine the effect of allergen-induced airway EOS on IL-17, subjects with mild allergic asthma underwent bronchoscopic segmental bronchoprovocation with allergen (SBP-Ag) after a treatment with an anti-IL-5 neutralizing antibody (mepolizumab) to reduce airway eosinophilia. IL-17 mRNA was measured in bronchoalveolar lavage (BAL) cells by qPCR. Results In vitro, EOS significantly increased IL-17 production by CD4+ T cells. Addition of exogenous IL-1ß increased expression of IL-17 mRNA by CD4+ T cells. EOS expressed and released IL-1ß. Furthermore, levels of IL-1ß in EOS supernatants highly correlated with their ability to increase IL-17 expression by CD4+ T cells, and neutralizing antibody to IL-1ß reduced expression of IL-17 mRNA. In vivo, reduction of EOS in the airway using mepolizumab was associated with diminished IL-17 expression after SBP-Ag. Conclusions and clinical relevance Our data demonstrate that EOS can promote IL-17 production through the release of IL-1ß. Enhanced IL-17 cytokine production is another mechanism by which EOS may participate in pathogenesis of allergic airway inflammation in asthma. [ABSTRACT FROM AUTHOR] )
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