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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...
Antibody Actions01:26

Antibody Actions

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.
Neutralization
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Enzyme-Linked Immunosorbent Assay

In 1971, Peter Perlman and Eva Engvall developed an Enzyme-linked immunosorbent assay (ELISA or EIA). ELISA differs from western blot in that the assays are conducted in microtiter plates or in vivo rather than on an absorbent membrane.
There are many different types of ELISAs, but they all involve an antibody molecule whose constant region binds an enzyme, leaving the variable region free to bind its specific antigen.  Enzyme-substrate reaction allows the antigen to be visualized or quantified.
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...

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Related Experiment Video

Updated: Jul 10, 2026

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

Detection of surface bound complement at increasing serum anticoagulant concentrations.

S Arvidsson1, A Askendal, T L Lindahl

  • 1Division of Applied Physics, Department of Physics, Chemistry and Biology, Linköping University, SE-581 83 Linköping, Sweden.

Colloids and Surfaces. B, Biointerfaces
|November 17, 2007
PubMed
Summary

Different anticoagulants impact antibody binding to complement factor C3c differently. High concentrations of heparin, dalteparin, and sodium citrate reduced binding, while fondaparinux showed no effect on this immune response.

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Area of Science:

  • Immunology
  • Biochemistry
  • Medical Diagnostics

Background:

  • Surface-mediated immune complement activation is crucial in various physiological and pathological processes.
  • Detecting complement activation often relies on antibody-based methods like ELISA, requiring careful consideration of sample handling.
  • Anticoagulants are routinely used in blood collection but can potentially interfere with immune assays.

Purpose of the Study:

  • To investigate the influence of common anticoagulants (heparin, dalteparin, fondaparinux, sodium citrate) on anti-complement factor 3c (anti-C3c) antibody binding.
  • To understand how these anticoagulants affect complement activation on a model surface (immobilized IgG) after incubation in human serum.
  • To determine if observed effects on antibody binding are due to complement depletion or direct interference with complement pathways.

Main Methods:

  • Incubation of immobilized IgG surfaces with human serum containing varying concentrations of heparin, dalteparin, fondaparinux, and sodium citrate.
  • Quantification of anti-C3c antibody binding using antibody-utilizing methods (specific method not detailed but implied by context).
  • Control experiments using EGTA-serum to differentiate pathway interference and C3a-des arg ELISA to assess complement depletion.

Main Results:

  • Anticoagulants demonstrated differential effects on anti-C3c antibody binding.
  • Increasing concentrations of heparin, dalteparin, and sodium citrate led to decreased anti-C3c binding.
  • Fondaparinux concentration did not significantly affect antibody deposition, and high anticoagulant levels were required to abolish binding.
  • Anticoagulants directly interfered with both the classical and alternative complement pathways, independent of complement depletion.

Conclusions:

  • The choice of anticoagulant can significantly alter the results of assays measuring surface-mediated complement activation.
  • Fondaparinux appears to have a minimal impact on complement activation detectable by anti-C3c binding under the tested conditions.
  • Understanding these anticoagulant-specific effects is critical for accurate interpretation of complement-based diagnostic assays.