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• W2016238035 abstract "Rationale: Th17 cells comprise a distinct lineage of proinflammatory T helper cells that are major contributors to allergic responses. It is unknown whether cyclooxygenase (COX)-derived eicosanoids regulate Th17 cells during allergic lung inflammation.Objectives: To determine the role of COX metabolites in regulating Th17 cell differentiation and function during allergic lung inflammation.Methods: COX-1−/−, COX-2−/−, and wild-type mice were studied in an in vivo model of ovalbumin-induced allergic inflammation and an in vitro model of Th17 differentiation using flow cytometry, cytokine assays, confocal microscopy, real-time polymerase chain reaction, and immunoblotting. In addition, the role of specific eicosanoids and their receptors was examined using synthetic prostaglandins (PGs), selective inhibitors, and siRNA knockdown.Measurements and Main Results: Th17 cell differentiation in lung, lymph nodes, and bronchoalveolar lavage fluid was significantly lower in COX-2−/− mice after ovalbumin sensitization and exposure in vivo. In vitro studies revealed significantly impaired Th17 cell differentiation of COX-2−/− naive CD4+ T cells with decreased Stat3 phosphorylation and RORγt expression. Synthetic PGF2α and PGI2 enhanced Th17 cell differentiation of COX-2−/− CD4+ T cells in vitro. The selective COX-2 inhibitor, NS-398, and PGF2α receptor and PGI2 receptor siRNA knockdown significantly decreased Th17 cell differentiation in vitro. Administration of synthetic PGs restored accumulation of Th17 cells in lungs of allergic COX-2−/− mice in vivo.Conclusions: COX-2 is a critical regulator of Th17 cell differentiation during allergic lung inflammation via autocrine signaling of PGI2 and PGF2α through their respective cell surface receptors." @default.
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• W2016238035 date "2011-07-01" @default.
• W2016238035 modified "2023-10-06" @default.
• W2016238035 title "Cyclooxygenase-2 Regulates Th17 Cell Differentiation during Allergic Lung Inflammation" @default.
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• W2016238035 doi "https://doi.org/10.1164/rccm.201010-1637oc" @default.
• W2016238035 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3172888" @default.
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