ArticleJournal of innate immunity2018
Kallikrein Cleaves C3 and Activates Complement.
Article in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 141 citations in OpenAlex.
- Prekallikrein: the catalytic crossroads of inflammation and thrombosis.Current opinion in hematology · 2026Review
- Comparative hemocompatibility assessment of fibrin/heparin-coated and PMEA-coated flow diverters.Journal of materials science. Materials in medicine · 2026Article
- Urokinase Promotes Redundantly Intratubular C3a-Formation But Not ENaC-Driven Hypertension in DOCA/Salt Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.Pflugers Archiv : European journal of physiology · 2026Article
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- Bacterial infection and activation of the contact pathway of coagulation.Blood vessels, thrombosis & hemostasis · 2025Review
- Article
- Granzyme K activates the entire complement cascade.Nature · 2025Article
- The role of the complement system in the response to cytotoxic therapy.Seminars in immunology · 2025Review
- Keratin 1 modulates intestinal barrier and immune responseWorld journal of gastroenterology · 2025Article
- Complement Factor B Deficiency Is Dispensable for Female Fertility but Affects Microbiome Diversity and Complement Activity.International journal of molecular sciences · 2025Article
- Candidiasis: Insights into Virulence Factors, Complement Evasion and Antifungal Drug Resistance.Microorganisms · 2025Review
- [Berberine ameliorates coronary artery endothelial cell injury in Kawasaki disease through complement and coagulation cascades].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Angiotensinogen and C3 compete for renin-induced complement activation.Frontiers in immunology · 2025Article
- Bradykinin B1 receptor signaling triggers complement activation on endothelial cells.Frontiers in immunology · 2025Article
- Infectious parvovirus B19 circulates in the blood coated with active host protease inhibitors.Nature communications · 2024Article
- Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024Review
- The Contrasting Effects ofToxins · 2024Article
- Local complement activation and modulation in mucosal immunity.Mucosal immunology · 2024Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human plasma contact system is an immune surveillance system activated by the negatively charged surfaces of bacteria and fungi and includes the kallikrein-kinin, the coagulation, and the fibrinolytic systems. Previous work shows that the contact system also activates complement, and that plasma enzymes like kallikrein, plasmin, thrombin, and FXII are involved in the activation process. Here, we show for the first time that kallikrein cleaves the central complement component C3 directly to yield active components C3b and C3a. The cleavage site within C3 is identical to that recognized by the C3 convertase. Also, kallikrein-generated C3b forms C3 convertases, which trigger the C3 amplification loop. Since kallikrein also cleaves factor B to yield Bb and Ba, kallikrein alone can trigger complement activation. Kallikrein-generated C3 convertases are inhibited by factor H; thus, the kallikrein activation pathway merges with the amplification loop of the alternative pathway. Taken together, these data suggest that activation of the contact system locally enhances complement activation on cell surfaces. The human pathogenic microbe Candida albicans activates the contact system in normal human serum. However, C. albicans immediately recruits factor H to the surface, thereby evading the alternative and likely kallikrein-mediated complement pathways.
Indexed as
Identifiers
What Socratic 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 Socratic graph.