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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...
Immunoglobulin-like Cell Adhesion Molecules01:31

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...
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
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...

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Related Experiment Video

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High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
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New perspectives on mannan-binding lectin-mediated complement activation.

Søren E Degn1, Steffen Thiel, Jens C Jensenius

  • 1Department of Medical Microbiology and Immunology, University of Aarhus, Denmark. sdegn@microbiology.au.dk

Immunobiology
|June 5, 2007
PubMed
Summary

The complement system, crucial for innate immunity, involves three pathways: classical, alternative, and lectin. Recent findings reveal bypass pathways, suggesting a complex network rather than linear routes.

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Published on: June 29, 2016

Area of Science:

  • Immunology
  • Innate Immunity
  • Complement System Biology

Background:

  • The complement system is vital for immune responses, with three known activation pathways: classical (CP), alternative (AP), and lectin (LP).
  • The LP is the least understood pathway.
  • CP and LP traditionally generate C3 convertase (C4bC2b), while bypass pathways activate C3 independently.

Purpose of the Study:

  • To explore the less-characterized lectin pathway (LP) of the complement system.
  • To investigate the existence and mechanisms of complement bypass pathways.
  • To re-evaluate the structural model of complement activation.

Main Methods:

  • Review and synthesis of existing literature on complement activation pathways.
  • Analysis of studies reporting complement bypass mechanisms.
  • Comparative analysis of standard and bypass complement activation routes.

Main Results:

  • The lectin pathway (LP) has recently been shown to possess a bypass mechanism.
  • This lectin bypass pathway requires mannan-binding lectin (MBL) and alternative pathway (AP) components.
  • Complement activation is better described as a scale-free network with C3 as a central hub, rather than three distinct linear pathways.

Conclusions:

  • The complement system is more complex than previously thought, featuring bypass pathways.
  • A network model, with C3 as a hub, better represents complement activation dynamics.
  • Further research into LP and bypass pathways is warranted for a comprehensive understanding of innate immunity.