ArticleThe Journal of allergy and clinical immunology2016
Distinct transcriptome profiles differentiate nonsteroidal anti-inflammatory drug-dependent from nonsteroidal anti-inflammatory drug-independent food-induced anaphylaxis.
Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Integrative transcriptomic analysis in human and mouse model of anaphylaxis identifies gene signatures associated with cell movement, migration and neuroinflammatory signalling.Frontiers in immunology · 2022Trial
- Food Allergen Component Sensitization Patterns in Eosinophilic Esophagitis: Insights from a Retrospective Comparative Study.Foods (Basel, Switzerland) · 2026Article
- Towards a Multi-omics Understanding of Anaphylaxis: Insights into Pathogenesis and Biomarker Identification.Clinical reviews in allergy & immunology · 2025Review
- The role of neutrophils in allergic disease.Clinical and experimental immunology · 2025Review
- Low Levels Matter: Clinical Relevance of Low Pru p 3 sIgE in Patients With Peach Allergy.Frontiers in allergy · 2022Article
- Lipid Ligands and Allergenic LTPs: Redefining the Paradigm of the Protein-Centered Vision in Allergy.Frontiers in allergy · 2022Review
- Adenosine Signaling in Mast Cells and Allergic Diseases.International journal of molecular sciences · 2021Review
- Dual transcriptomic and epigenomic study of reaction severity in peanut-allergic children.The Journal of allergy and clinical immunology · 2020Article
- Immune-Mediated Mechanisms in Cofactor-Dependent Food Allergy and Anaphylaxis: Effect of Cofactors in Basophils and Mast Cells.Frontiers in immunology · 2020Review
- [Personalized medicine in allergology].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2019Review
- The Mast Cell, Contact, and Coagulation System Connection in Anaphylaxis.Frontiers in immunology · 2017Review
- Alternative Anaphylactic Routes: The Potential Role of Macrophages.Frontiers in immunology · 2017Review
- How to manage anaphylaxis in primary care.Clinical and translational allergy · 2017Review
- Mechanisms, Cofactors, and Augmenting Factors Involved in Anaphylaxis.Frontiers in immunology · 2017Review
- Guidelines for the use and interpretation of diagnostic methods in adult food allergy.Clinical and molecular allergy : CMA · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
backgroundLipid transfer protein (LTP), an abundant protein in fruits, vegetables, and nuts, is a common food allergen in Mediterranean areas causing diverse allergic reactions. Approximately 40% of food-related anaphylaxis induced by LTPs requires nonsteroidal anti-inflammatory drugs (NSAIDs) as a triggering cofactor.
objectiveWe sought to better understand the determinants of NSAID-dependent and NSAID-independent LTP-induced anaphylaxis (LTP-A).
methodsSelection of patients was based on a proved clinical history of NSAID-dependent or NSAID-independent anaphylaxis to LTPs, positive skin prick test response to LTPs, and serum LTP IgE. Whole-transcriptome (RNA sequencing) analysis of blood cells from 14 patients with NSAID-related LTP-A (NSAID-LTP-A), 7 patients with LTP-A, and 13 healthy control subjects was performed to identify distinct gene expression signatures.
resultsExpression of genes regulating gastrointestinal epithelial renewal was altered in both patient sets, particularly in those with LTP-A, who also presented with gene expression profiles characteristic of an inflammatory syndrome. These included altered B-cell pathways, increased neutrophil activation markers, and increased reactive oxygen species levels. Increased expression of the IgG receptor (CD64) in patients with LTP-A was mirrored by the presence of LTP-specific IgG1 and IgG3. Conversely, patients with NSAID-LTP-A were characterized by reduced expression of IFN-γ-regulated genes and IFN-γ levels, as well as upregulated expression of adenosine receptor 3 (ADORA3) and genes related to adenosine metabolism.
conclusionsGene ontology analysis suggests disturbances in gut epithelial homeostasis in both groups with LTP-A, with potential integrity breaches in patients with LTP-A that might explain their distinct inflammatory signatures. Differential regulation in patients with LTP-A and those with NSAID-LTP-A of the IFN-γ pathway, IgG receptors, and ADORA3 might provide the pathogenic basis of their distinct responses.
Indexed as
Identifiers
What OpenQuestion holds
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.