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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...
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
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...
Global Regulatory Systems01:28

Global Regulatory Systems

Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

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Related Experiment Video

Updated: Jul 18, 2026

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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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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Solid-phase classical complement activation by C-reactive protein (CRP) is inhibited by fluid-phase CRP-C1q

Christopher Sjöwall1, Jonas Wetterö, Torbjörn Bengtsson

  • 1Division of Rheumatology/AIR, Department of Molecular and Clinical Medicine, Linköping University, SE-581 85 Linköping, Sweden. chrsj@imk.liu.se

Biochemical and Biophysical Research Communications
|November 23, 2006
PubMed
Summary

C-reactive protein (CRP) binding to surfaces triggers complement activation. However, high CRP levels paradoxically down-regulate this activation through interaction with C1q, suggesting a novel regulatory mechanism.

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Published on: May 19, 2020

Area of Science:

  • Immunology
  • Biochemistry

Background:

  • C-reactive protein (CRP) interactions with various molecules are known, but its precise biological roles, particularly in complement activation, remain unclear.
  • Understanding CRP's function is crucial for deciphering immune responses and associated pathologies.

Purpose of the Study:

  • To investigate and characterize C-reactive protein (CRP)-induced complement activation using ellipsometry.
  • To elucidate the dose-dependent effects of CRP on the classical complement pathway.

Main Methods:

  • Immobilization of phosphorylcholine (PC) conjugated with keyhole limpet hemocyanin (PC-KLH) onto cross-linked fibrinogen.
  • Exposure of low-CRP serum with varying added CRP concentrations to PC-KLH surfaces.
  • Quantification of total serum protein deposition and specific detection of IgG, C1q, C3c, C4, factor H, and CRP using polyclonal antibodies.

Main Results:

  • CRP binding to PC-KLH surfaces dose-dependently initiated classical complement pathway activation.
  • Complement activation was unexpectedly inhibited at CRP concentrations exceeding 150 mg/L.
  • Radial immunodiffusion revealed CRP-C1q interaction in serum samples with high CRP levels.

Conclusions:

  • CRP binding to surfaces triggers classical complement pathway activation, but high CRP concentrations lead to down-regulation via fluid-phase CRP-C1q interaction.
  • This interaction represents a potential new level of complement regulation.
  • Findings have implications for understanding conditions like systemic lupus erythematosus, where CRP levels can be atypical during disease flares.