ArticleClinical and experimental medicine2018
The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema.
Article in Clinical and experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Mast cell mediators in hereditary angioedema.Orphanet journal of rare diseases · 2026Article
- Associations of hereditary angioedema attacks with intestinal permeability and inflammatory cytokines.Frontiers in immunology · 2026Article
- Activation of the Complement/Lectin Pathway, Angiopoietin/Tie-2/VEGF-System, Cytokines and Chemokines in Different Angioedema Subtypes.European journal of immunology · 2025Article
- Systemic inflammation biomarkers during angioedema attacks in hereditary angioedema.Frontiers in immunology · 2024Article
- Hereditary angioedema plasma proteomics following specific plasma kallikrein inhibition with lanadelumab.Frontiers in immunology · 2024Article
- Increased thromboinflammatory load in hereditary angioedema.Clinical and experimental immunology · 2023Article
- PLAUR splicing pattern in hereditary angioedema patients' monocytes and macrophages.Molecular biology reports · 2023Article
- Altered Urinary Metabolomics in Hereditary Angioedema.Metabolites · 2022Article
- The Role of Bradykinin Receptors in Hereditary Angioedema Due to C1-Inhibitor Deficiency.International journal of molecular sciences · 2022Article
- Roles of Immune Cells in Hereditary Angioedema.Clinical reviews in allergy & immunology · 2021Review
- Epigenetic alterations on C1-inhibitor expression may influence hereditary angioedema attack frequency and C4 levels: Comment on: Karagianni P, Goules AV, Tzioufas AG. Epigenetic alterations in Sjogren's syndrome patient saliva.Clinical and experimental immunology · 2020Article
- Does hereditary angioedema make COVID-19 worse?The World Allergy Organization journal · 2020Review
- Polyphosphate as a Target for Interference With Inflammation and Thrombosis.Frontiers in medicine · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary angioedema (HAE) is a rare autosomic-dominant disorder characterized by a deficiency of C1 esterase inhibitor which causes episodic swellings of subcutaneous tissues, bowel walls and upper airways that are disabling and potentially life-threatening. We evaluated n = 17 patients with confirmed HAE diagnosis during attack and remission state and n = 19 healthy subjects. The samples were tested for a panel of IL (Interleukin)-17-type cytokines (IL-1β, IL-6, IL-10, granulocyte-macrophage colony stimulating factor (GM-CSF), IL-17, IL-21, IL-22, IL-23) and transforming growth factor-beta (TGF-β) subtypes. Data indicate that there are variations of cytokine levels in HAE subjects comparing the condition during the crisis respect to the value in the remission phase, in particular type 17 signature cytokines are increased, whereas IL-23 is unmodified and TGF-β3 is significantly reduced. When comparing healthy and HAE subjects in the remission state, we found a significant difference for IL-17, GM-CSF, IL-21, TGF-β1 and TGF-β2 cytokines. These results confirm and extend our previous findings indicating that in HAE there is operating an inflammatory activation process, which involves also T helper 17 (Th17) cytokines and TGF-β isoforms, associated with localized angioedema attacks and characterized by elevated bradykinin levels.
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