Anti-interleukin-33 inhibits cigarette smoke-induced lung inflammation in mice
Published 2012 View Full Article
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Title
Anti-interleukin-33 inhibits cigarette smoke-induced lung inflammation in mice
Authors
Keywords
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Journal
IMMUNOLOGY
Volume 138, Issue 1, Pages 76-82
Publisher
Wiley
Online
2012-10-19
DOI
10.1111/imm.12020
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Note: Only part of the references are listed.- IL-33 Induces Antigen-Specific IL-5+ T Cells and Promotes Allergic-Induced Airway Inflammation Independent of IL-4
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- Transcriptional Regulation of Murine IL-33 by TLR and Non-TLR Agonists
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- Stimulation of Ly-6G on neutrophils in LPS-primed mice induces platelet-activating factor (PAF)-mediated anaphylaxis-like shock
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- IL-33 induces neutrophil migration in rheumatoid arthritis and is a target of anti-TNF therapy
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- IL-33 Is Produced by Mast Cells and Regulates IgE-Dependent Inflammation
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- Anti-IL-33 antibody treatment inhibits airway inflammation in a murine model of allergic asthma
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- Increased soluble serum markers caspase-cleaved cytokeratin-18, histones, and ST2 indicate apoptotic turnover and chronic immune response in COPD
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- Administration of IL-33 induces airway hyperresponsiveness and goblet cell hyperplasia in the lungs in the absence of adaptive immune system
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- IL-33 amplifies both Th1- and Th2-type responses through its activity on human basophils, allergen-reactive Th2 cells, iNKT and NK Cells
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- IL-33 exacerbates antigen-induced arthritis by activating mast cells
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