ArticleFrontiers in immunology2023
Key genes and immune infiltration in chronic spontaneous urticaria: a study of bioinformatics and systems biology.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 11 citations in OpenAlex.
- Development and validation of a clinically applicable biomarker panel for identifying autoimmune type IIb chronic spontaneous urticaria.The World Allergy Organization journal · 2026Article
- Immune cells influence chronic spontaneous urticaria by inflammatory proteins: Mendelian randomization and bioinformatic analysis.The journal of allergy and clinical immunology. Global · 2026Article
- Identification of oxidative stress-related hub genes and immune infiltration characterization in chronic spontaneous urticaria.Molecular genetics and genomics : MGG · 2026Article
- Lactobacillus paragasseri LG-1 Alleviates Urticaria-Like Symptoms in Mice via Modulation of Gut Microbiota, Hypoxanthine and Uric Acid.Microbial biotechnology · 2026Article
- Therapeutic expansion of JAK inhibitors in Chinese dermatological practice: beyond atopic dermatitis to novel autoimmune frontiers.Frontiers in medicine · 2026Review
- T Cell/Mast Cell Crosstalk in the Skin of Patients Suffering From Immune-Mediated Diseases, Focusing on Chronic Spontaneous Urticaria.Clinical and translational allergy · 2026Review
- Elucidating the Mechanism of Xiaoqinglong Decoction in Chronic Urticaria Treatment: An Integrated Approach of Network Pharmacology, Bioinformatics Analysis, Molecular Docking, and Molecular Dynamics Simulations.Current computer-aided drug design · 2026Article
- Distinct Cytokine Profiles in Chronic Spontaneous Urticaria Refractory to H1-Antihistamines Compared to Healthy Controls.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- Association Between Proinflammatory Cytokines IL-6 and TNF-Alpha, Psychological Stress and Chronic Spontaneous Urticaria Severity.International journal of molecular sciences · 2025Article
- Identification of immune-associated biomarkers in diagnosing allergic rhinitis.The World Allergy Organization journal · 2025Article
- Is there a role of genetics in acute and chronic urticaria-A systematic review and meta-analysis.Clinical and translational allergy · 2025Article
- Unveiling the immunopharmacological mechanisms of Danggui Yinzi (DGYZ) in treating chronic urticaria: insights from network pharmacology and experimental validation.Chinese medicine · 2025Article
- A pharmacovigilance analysis of abrocitinib-related skin adverse events based on the FDA Adverse Event Reporting System (FAERS).Archives of dermatological research · 2025Article
- Bioinformatics analysis combined with untargeted metabolomics reveals lipid metabolism-related genes and their biological markers in chronic spontaneous urticaria.Frontiers in genetics · 2025Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic spontaneous urticaria (CSU) is defined by the spontaneous occurrence of wheals and/or angioedema for >6 weeks. The pathogenesis involves skin mast cells, but the complex causes of their activation remain to be characterized in detail. Objectives: To explore disease-driving genes and biological pathways in CSU. Methods: Two microarray data sets, e.g., GSE57178 and GSE72540, with mRNA information of skin from CSU patients, were downloaded from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, co-expression and drug prediction analysis, and immune and stromal cells deconvolution analyses were applied to identify hub genes and key drivers of CSU pathogenesis. Results: In total, we identified 92 up-regulated and 7 down-regulated genes in CSU lesions. These were significantly enriched in CSU-related pathways such as TNF, NF-κB, and JAK-STAT signaling. Based on PPI network modeling, four genes, i.e., IL-6, TLR-4, ICAM-1, and PTGS-2, were computationally identified as key pathogenic players in CSU. Immune infiltration analyses indicated that dendritic cells, Th2 cells, mast cells, megakaryocyte-erythroid progenitor, preadipocytes, and M1 macrophages were increased in lesional CSU skin. Conclusion: Our results offer new insights on the pathogenesis of CSU and suggest that TNF, NF-κB, JAK-STAT, IL-6, TLR-4, ICAM-1, and PTGS-2 may be candidate targets for novel CSU treatments.
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