ArticleThe Journal of allergy and clinical immunology2015
Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells.
Article in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Genetic and environmental risk factors of asthma: a narrative review.Frontiers in immunology · 2026Pooled it
- Inhaled siRNA therapy targeting RAGE for pulmonary inflammation: a first-in-human randomized trial.Nature medicine · 2026Trial
- AGE-RAGE Axis Involvement in Allergies and Autoimmunity: Cellular Signaling, Barrier Dysfunction and Immune Polarization.Biomolecules · 2026Review
- From gut microbiota dysbiosis to immune dysregulation: pathogenic mechanisms and emerging therapeutic perspectives in pediatric asthma.Frontiers in immunology · 2026Review
- Dietary advanced glycation end-products promote food allergy by disrupting intestinal barrier and enhancing Th2 immunity.Nature communications · 2025Article
- Functional Characterization of Glycated Peptide Aggregates in Whey Protein Hydrolysates.Food science & nutrition · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Epithelial sensing in allergic disease.Current opinion in immunology · 2024Review
- Differential proteins from EVs identification based on tandem mass tags analysis and effect of Treg-derived EVs on T-lymphocytes in COPD patients.Respiratory research · 2024Article
- Breathing new life into the study of COPD with genes identified from genome-wide association studies.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- The AGE-RAGE axis associates with chronic pulmonary diseases and smoking in the Rotterdam study.Respiratory research · 2024Article
- S100A alarmins and thymic stromal lymphopoietin (TSLP) regulation in severe asthma following bronchial thermoplasty.Respiratory research · 2023Article
- Determination of the effects of advanced glycation end products receptor polymorphisms and its activation on structural cell responses and inflammation in asthma.Turkish journal of medical sciences · 2023Article
- Alarmins and MicroRNAs, a New Axis in the Genesis of Respiratory Diseases: Possible Therapeutic Implications.International journal of molecular sciences · 2023Review
- RAGE contributes to allergen driven severe neutrophilic airway inflammationFrontiers in immunology · 2023Article
- How does cigarette smoking affect airway remodeling in asthmatics?Tobacco induced diseases · 2023Review
- Do advanced glycation end products contribute to food allergy?Frontiers in allergy · 2023Review
- A genomic approach identifies sRAGE as a putatively causal protein for asthma.The Journal of allergy and clinical immunology · 2022Article
- Neutrophils and Asthma.Diagnostics (Basel, Switzerland) · 2022Review
- RAGE mediates airway inflammation via the HDAC1 pathway in a toluene diisocyanate-induced murine asthma model.BMC pulmonary medicine · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSingle nucleotide polymorphisms in the human gene for the receptor for advanced glycation end-products (RAGE) are associated with an increased incidence of asthma. RAGE is highly expressed in the lung and has been reported to play a vital role in the pathogenesis of murine models of asthma/allergic airway inflammation (AAI) by promoting expression of the type 2 cytokines IL-5 and IL-13. IL-5 and IL-13 are prominently secreted by group 2 innate lymphoid cells (ILC2s), which are stimulated by the proallergic cytokine IL-33.
objectiveWe sought to test the hypothesis that pulmonary RAGE is necessary for allergen-induced ILC2 accumulation in the lung.
methodsAAI was induced in wild-type and RAGE knockout mice by using IL-33, house dust mite extract, or Alternaria alternata extract. RAGE's lung-specific role in type 2 responses was explored with bone marrow chimeras and induction of gastrointestinal type 2 immune responses.
resultsRAGE was found to drive AAI by promoting IL-33 expression in response to allergen and by coordinating the inflammatory response downstream of IL-33. Absence of RAGE impedes pulmonary accumulation of ILC2s in models of AAI. Bone marrow chimera studies suggest that pulmonary parenchymal, but not hematopoietic, RAGE has a central role in promoting AAI. In contrast to the lung, the absence of RAGE does not affect IL-33-induced ILC2 influx in the spleen, type 2 cytokine production in the peritoneum, or mucus hypersecretion in the gastrointestinal tract.
conclusionsFor the first time, this study demonstrates that a parenchymal factor, RAGE, mediates lung-specific accumulation of ILC2s.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.