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Related Concept Videos

Complement System01:27

Complement System

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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...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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Antibody Actions01:26

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Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
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Antimicrobial Proteins01:23

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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.
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Defense Against Bacterial Pathogens01:31

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Related Experiment Video

Updated: Feb 17, 2026

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

Published on: January 29, 2014

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Kallikrein Cleaves C3 and Activates Complement.

Sarah Irmscher1, Nadia Döring, Luke D Halder

  • 1Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany.

Journal of Innate Immunity
|December 14, 2017
PubMed
Summary
This summary is machine-generated.

Kallikrein, a plasma enzyme, directly activates complement by cleaving C3, initiating immune responses. This pathway merges with the alternative complement pathway but can be evaded by microbes like Candida albicans.

Keywords:
<italic>Candida albicans</italic>Complement systemContact activationFactor HHost defenseKallikrein

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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
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Area of Science:

  • Immunology
  • Biochemistry

Background:

  • The human plasma contact system is a key immune surveillance mechanism.
  • It interacts with the coagulation and fibrinolytic systems.
  • Previous studies indicated its role in complement activation via enzymes like kallikrein.

Purpose of the Study:

  • To investigate the direct interaction between kallikrein and the complement system.
  • To elucidate the mechanism by which kallikrein activates complement component C3.

Main Methods:

  • Enzymatic assays to demonstrate kallikrein's cleavage of C3.
  • Analysis of cleavage sites and generated complement components.
  • Investigation of factor B cleavage by kallikrein.
  • Assessment of complement activation in the presence of factor H.

Main Results:

  • Kallikrein directly cleaves C3 at the same site as the C3 convertase, producing active C3b and C3a.
  • Kallikrein-generated C3b forms functional C3 convertases, initiating a C3 amplification loop.
  • Kallikrein also cleaves factor B, enabling it to trigger complement activation independently.
  • This kallikrein-mediated pathway is regulated by factor H, integrating with the alternative complement pathway.

Conclusions:

  • Kallikrein directly activates the complement system by cleaving C3, enhancing local complement activation on cell surfaces.
  • This newly identified pathway merges with the alternative complement pathway.
  • Pathogenic microbes like Candida albicans can evade this pathway by recruiting factor H.