ReviewFrontiers in immunology2017
Factor XII-Driven Inflammatory Reactions with Implications for Anaphylaxis.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- Drug-induced anaphylaxis: Molecular pathophysiology, diagnosis, and management.Asia Pacific allergy · 2026Article
- Chemical Profiling and Multimodal Anti-Inflammatory Activity ofMolecules (Basel, Switzerland) · 2026Article
- Behavioural withdrawal during an acute stress test as a marker of psychobiological vulnerability in hereditary angioedema.Frontiers in immunology · 2026Article
- Discovery of a new lead molecule to develop a novel class of human factor XIIa inhibitors.Journal of thrombosis and thrombolysis · 2024Article
- Pseudo-allergic reactions induced by Chinese medicine injections: a review.Chinese medicine · 2023Review
- MASP2 inhibition by narsoplimab suppresses endotheliopathies characteristic of transplant-associated thrombotic microangiopathy: in vitro and ex vivo evidence.Clinical and experimental immunology · 2023Article
- Safety of mRNA COVID-19 vaccinations in patients with allergic diseases.Public health in practice (Oxford, England) · 2023Article
- Factor XII contributes to thrombotic complications and vaso-occlusion in sickle cell disease.Blood · 2023Article
- 6-(Arylaminomethyl) Isoquinolines as Enzyme Inhibitors and Their Preparation: A Patent Highlight of Factor XIIa Inhibitors.Cardiovascular & hematological agents in medicinal chemistry · 2023Article
- In vitro and in vivo anti-inflammatory and anticoagulant activities of Myrciaria plinioides D. Legrand ethanol leaf extract.Inflammopharmacology · 2022Article
- Contact pathway in surgical and transcatheter aortic valve replacement.Frontiers in cardiovascular medicine · 2022Article
- Pathophysiological, Cellular, and Molecular Events of the Vascular System in Anaphylaxis.Frontiers in immunology · 2022Review
- Identification of the factor XII contact activation site enables sensitive coagulation diagnostics.Nature communications · 2021Article
- Effect ofBiology · 2021Article
- Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond.International journal of molecular sciences · 2021Review
- Potential mechanisms of anaphylaxis to COVID-19 mRNA vaccines.The Journal of allergy and clinical immunology · 2021Review
- Plasmin, Immunity, and Surgical Site Infection.Journal of clinical medicine · 2021Review
- Proteomic and Biological Analysis of anFrontiers in immunology · 2021Article
- Penicillin causes non-allergic anaphylaxis by activating the contact system.Scientific reports · 2020Article
- Extracellular RNA as a Versatile DAMP and Alarm Signal That Influences Leukocyte Recruitment in Inflammation and Infection.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaphylaxis is a life-threatening allergic reaction. It is triggered by the release of pro-inflammatory cytokines and mediators from mast cells and basophils in response to immunologic or non-immunologic mechanisms. Mediators that are released upon mast cell activation include the highly sulfated polysaccharide and inorganic polymer heparin and polyphosphate (polyP), respectively. Heparin and polyP supply a negative surface for factor XII (FXII) activation, a serine protease that drives contact system-mediated coagulation and inflammation. Activation of the FXII substrate plasma kallikrein leads to further activation of zymogen FXII and triggers the pro-inflammatory kallikrein-kinin system that results in the release of the mediator bradykinin (BK). The severity of anaphylaxis is correlated with the intensity of contact system activation, the magnitude of mast cell activation, and BK formation. The main inhibitor of the complement system, C1 esterase inhibitor, potently interferes with FXII activity, indicating a meaningful cross-link between complement and kallikrein-kinin systems. Deficiency in a functional C1 esterase inhibitor leads to a severe swelling disorder called hereditary angioedema (HAE). The significance of FXII in these disorders highlights the importance of studying how these processes are integrated and can be therapeutically targeted. In this review, we focus on how FXII integrates with inflammation and the complement system to cause anaphylaxis and HAE as well as highlight current diagnosis and treatments of BK-related diseases.
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