Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Antimicrobial Proteins01:23

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Elucidating allergic reaction mechanisms in response to SARS-CoV-2 mRNA vaccination in adults.

Allergy·2024
Same author

A Monoclonal Antibody That Provides a Model for C3 Nephritic Factors.

Monoclonal antibodies in immunodiagnosis and immunotherapy·2023
Same author

Deep phenotyping detects a pathological CD4<sup>+</sup> T-cell complosome signature in systemic sclerosis.

Cellular & molecular immunology·2020
Same author

Complement activation on neutrophils initiates endothelial adhesion and extravasation.

Molecular immunology·2019
Same author

Timing and mechanism of conceptus demise in a complement regulatory membrane protein deficient mouse.

American journal of reproductive immunology (New York, N.Y. : 1989)·2018
Same author

Contribution of Adipose-Derived Factor D/Adipsin to Complement Alternative Pathway Activation: Lessons from Lipodystrophy.

Journal of immunology (Baltimore, Md. : 1950)·2018

Related Experiment Video

Updated: Jul 7, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Properdin and complement activation: a fresh perspective.

Dennis E Hourcade1

  • 1Washington University School of Medicine, Department of Medicine/Division of Rheumatology, St. Louis, MO 63110-1093, USA. dhourcad@im.wustl.edu

Current Drug Targets
|February 22, 2008
PubMed
Summary

Properdin stabilizes complement C3 convertases in the alternative pathway and also initiates new convertase assembly on microbial surfaces. This dual role necessitates reassessing complement activation in autoimmune diseases and host defense.

More Related Videos

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Related Experiment Videos

Last Updated: Jul 7, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Area of Science:

  • Immunology
  • Molecular Biology
  • Biochemistry

Background:

  • Complement C3 convertases are key proteases in the complement cascade.
  • Properdin's role in stabilizing the alternative pathway convertase is well-known.
  • New evidence suggests properdin also initiates de novo convertase assembly on microbial surfaces.

Purpose of the Study:

  • To investigate the dual role of properdin in complement activation.
  • To differentiate the alternative pathway from the properdin-directed pathway.
  • To explore therapeutic strategies targeting properdin's functions.

Main Methods:

  • Biochemical assays to study C3 convertase assembly.
  • Surface binding studies of properdin on microbial surfaces.
  • Functional assays to assess complement activation pathways.

Main Results:

  • Properdin binds microbial surfaces, facilitating de novo C3 convertase assembly.
  • Properdin mediates complement activation through both the alternative and a new properdin-directed pathway.
  • Previous studies could not distinguish between these two pathways.

Conclusions:

  • Properdin plays a critical role in at least two distinct complement activation pathways.
  • Understanding these pathways is crucial for differentiating their roles in disease and host defense.
  • Targeting properdin offers potential therapeutic avenues for autoimmune diseases and infections.