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IL-6 prevents Th2 cell polarization by promoting SOCS3-dependent suppression of IL-2 signaling
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作者 Holly Bachus Erin McLaughlin +6 位作者 Crystal Lewis Amber M.Papillion Etty N.Benveniste dave durell hill Alexander F.Rosenberg AndréBallesteros-Tato Beatriz León 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2023年第6期651-665,共15页
Defective interleukin-6 (IL-6) signaling has been associated with Th2 bias and elevated IgE levels. However, the underlying mechanism by which IL-6 prevents the development of Th2-driven diseases remains unknown. Usin... Defective interleukin-6 (IL-6) signaling has been associated with Th2 bias and elevated IgE levels. However, the underlying mechanism by which IL-6 prevents the development of Th2-driven diseases remains unknown. Using a model of house dust mite (HDM)-induced Th2 cell differentiation and allergic airway inflammation, we showed that IL-6 signaling in allergen-specific T cells was required to prevent Th2 cell differentiation and the subsequent IgE response and allergic inflammation. Th2 cell lineage commitment required strong sustained IL-2 signaling. We found that IL-6 turned off IL-2 signaling during early T-cell activation and thus inhibited Th2 priming. Mechanistically, IL-6-driven inhibition of IL-2 signaling in responding T cells was mediated by upregulation of Suppressor Of Cytokine Signaling 3 (SOCS3). This mechanism could be mimicked by pharmacological Janus Kinase-1 (JAK1) inhibition. Collectively, our results identify an unrecognized mechanism that prevents the development of unwanted Th2 cell responses and associated diseases and outline potential preventive interventions. 展开更多
关键词 Th2 cell polarization IL-6 IL-2 SOCS3 JAK1 inhibitor
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