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

12.9K
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...
12.9K
Renal Corpuscle01:20

Renal Corpuscle

9.6K
The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
Glomerulus: Structure and Function
The glomerulus is a tiny, intricate network of capillaries located at the beginning of the nephron. It's enveloped by the Bowman's capsule and receives its blood supply from an afferent arteriole, which divides into numerous...
9.6K
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

150
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...
150
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

207
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...
207
Complementation Tests00:49

Complementation Tests

6.6K
A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
6.6K
Antibody Actions01:26

Antibody Actions

4.1K
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...
4.1K

You might also read

Related Articles

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

Sort by
Same author

<i>Moss-derived</i> recombinant Factor H, CPV-104, effectively antagonizes alternative pathway C3/C5 convertases stabilization by NeFs from patients with primary C3 glomerulopathy.

Frontiers in immunology·2026
Same author

Complement-Mediated Postpartum Atypical Hemolytic Uremic Syndrome With Collapsing Focal Segmental Glomerulosclerosis Associated With a Novel CFHR5 Copy Number Variant.

American journal of kidney diseases : the official journal of the National Kidney Foundation·2026
Same author

A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.

Frontiers in immunology·2026
Same author

Response to the Letter to the Editor Entitled "Defining "Dominance" in Atypical Hemolytic Uremic Syndrome: Distinguishing Amplification From Initiation".

Kidney international reports·2026
Same author

Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis.

Frontiers in immunology·2026
Same author

Deletion of the Mouse Homolog of Human FHR1 (muFHR1) Alleviates Atherosclerosis in ApoE-/- mice.

International journal of medical sciences·2026

Related Experiment Video

Updated: Apr 13, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

12.3K

The role of complement in C3 glomerulopathy.

Peter F Zipfel1, Christine Skerka2, Qian Chen2

  • 1Leibniz Institute for Natural Product Research and Infection Biology, Jena, Germany; Friedrich Schiller University Jena, Germany.

Molecular Immunology
|May 2, 2015
PubMed
Summary

C3 glomerulopathy involves kidney damage due to complement system dysregulation, characterized by C3 fragment deposition without significant immunoglobulin presence. Further research is needed to understand disease mechanisms, identify biomarkers, and develop effective treatments.

Keywords:
C3 nephritic factorComplement C3 glomerulopathyDense deposit diseasesMPGN membranoproliferative

More Related Videos

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

31.4K
A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
10:05

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

Published on: March 18, 2021

7.7K

Related Experiment Videos

Last Updated: Apr 13, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

12.3K
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

31.4K
A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
10:05

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures

Published on: March 18, 2021

7.7K

Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • C3 glomerulopathy is a kidney disease defined by C3 fragment deposition in glomeruli, with minimal immunoglobulin presence.
  • The complement system, a crucial part of innate immunity, regulates inflammation and pathogen defense but can cause damage if dysregulated.
  • Current understanding of C3 glomerulopathy pathogenesis, biomarkers, and treatments remains limited.

Purpose of the Study:

  • To elucidate the underlying disease mechanisms of C3 glomerulopathy.
  • To identify precise biomarkers for diagnosis and monitoring.
  • To explore potential therapeutic strategies for C3 glomerulopathy.

Main Methods:

  • Kidney biopsy analysis including histological, immunohistological, and electron microscopy.
  • Investigation of complement system activation pathways and regulatory mechanisms.
  • Analysis of C3 cleavage product deposition and its correlation with glomerular damage.

Main Results:

  • C3 glomerulopathy is characterized by glomerular accumulation of C3 cleavage fragments.
  • Defective regulation of the complement system's alternative pathway is implicated.
  • The precise mechanisms linking C3 deposition to glomerular injury are not fully defined.

Conclusions:

  • C3 glomerulopathy requires further investigation into its complex pathogenic mechanisms.
  • Developing specific biomarkers is essential for accurate diagnosis and prognosis.
  • Targeting complement system dysregulation offers a potential therapeutic avenue.