ArticleMucosal immunology2024
Itaconate suppresses house dust mite-induced allergic airways disease and Th2 cell differentiation.
Article in Mucosal immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Article
- Protective role of IRG1/itaconate in acute myocardial injury: association with NLRP3 inflammasome and oxidative stress.Scientific reports · 2026Article
- Metabolomic and immunological signatures of asthma severity in children.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025Article
- Reprogramming immunity with itaconate: metabolic mechanisms and therapeutic perspectives.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Elevated GFI1 in Alveolar Macrophages Suppresses ACOD1 Expression and Exacerbates Lipopolysaccharide-Induced Lung Injury in Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Immunometabolic programming of macrophages in asthma pathogenesis and therapy.Frontiers in physiology · 2025Review
- Elevated SerpinB2 regulates MUC5AC expression via STAT6 signaling in nasal epithelial cells in allergic rhinitis.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Itaconate was initially identified as an antimicrobial compound produced by myeloid cells. Beyond its antimicrobial role, itaconate may also serve as a crucial metabolic and immune modulator. We therefore examined the roles of aconitate decarboxylase 1 (Acod1) and itaconate in house dust mite (HDM)-sensitized and -challenged mice, a model of T helper 2 (Th2)-driven allergic airways disease. HDM treatment induced lung Acod1 mRNA expression and bronchoalveolar lavage (BAL) itaconate levels in wild-type C57BL/6 mice. Acod1 knockout mice (Acod1-KO) with negligible BAL itaconate showed heightened HDM-induced type 2 cytokine expression, increased serum IgE, and enhanced recruitment of Th2 cells in the lung, indicating a shift towards a more pronounced Th2 immune response. Acod1-KO mice also showed increased eosinophilic airway inflammation and hyperresponsiveness. Experiments in chimeric mice demonstrated that bone marrow from Acod1-KO mice is sufficient to increase type 2 cytokine expression in wild-type mice, and that restitution of bone marrow from wild type mice attenuates mRNA expression of Th2 cytokines in Acod1-KO mice. Specific deletion of Acod1 in lysozyme-secreting macrophages (LysM-cre
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