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

Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

96
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...
96
Complement System01:27

Complement System

12.0K
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...
12.0K
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

89
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...
89
Humoral Immune Responses01:36

Humoral Immune Responses

85.6K
Overview
85.6K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

2.3K
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...
2.3K
Protein Complex Assembly02:41

Protein Complex Assembly

17.0K
Proteins can form homomeric complexes with another unit of the same protein or heteromeric complexes with different types.  Most protein complexes self-assemble spontaneously via ordered pathways, while some proteins need assembly factors that guide their proper assembly. Despite the crowded intracellular environment, proteins usually interact with their correct partners and form functional complexes.
Many viruses self-assemble into a fully functional unit using the infected host cell to...
17.0K

You might also read

Related Articles

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

Sort by
Same author

Age at onset and cumulative initial prednisolone dose predict frequent relapses in steroid-sensitive nephrotic syndrome: an individual participant data systematic review and meta-analysis of placebo-controlled RCTs.

Pediatric nephrology (Berlin, Germany)·2026
Same author

A systematic review of short-term outcomes in patients with anti-factor H associated atypical HUS managed with plasma exchanges versus eculizumab.

Pediatric nephrology (Berlin, Germany)·2026
Same author

Pediatric Nephrology in Clinical Practice.

Indian journal of pediatrics·2026
Same author

Optimizing Large-Volume Paracentesis in a Gastroenterology Ward: A Two-Cycle Quality Improvement Project.

Cureus·2026
Same author

Rituximab-induced hypogammaglobulinemia in childhood nephrotic syndrome: a systematic review and meta-analysis.

European journal of pediatrics·2026
Same author

CAKUT: Current Understanding and Future Directions.

Indian journal of pediatrics·2026

Related Experiment Video

Updated: Mar 17, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
09:37

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

8.9K

Anti-complement-factor H-associated glomerulopathies.

Marie-Agnes Dragon Durey1,2,3, Aditi Sinha4, Shambhuprasad Kotresh Togarsimalemath1,2

  • 1INSERM UMRS1138, Centre de Recherche des Cordeliers, Université Pierre et Marie Curie, 15 rue de l'ecole de medecine, 75006 Paris, France.

Nature Reviews. Nephrology
|July 26, 2016
PubMed
Summary
This summary is machine-generated.

Autoantibodies against complement factor H (FH) cause atypical hemolytic uremic syndrome (aHUS), leading to kidney injury. Treatment with plasma exchange and immunosuppression effectively manages aHUS associated with FH autoantibodies.

More Related Videos

Enrichment of Bruch's Membrane from Human Donor Eyes
10:22

Enrichment of Bruch's Membrane from Human Donor Eyes

Published on: November 15, 2015

12.6K
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

31.3K

Related Experiment Videos

Last Updated: Mar 17, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
09:37

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

8.9K
Enrichment of Bruch's Membrane from Human Donor Eyes
10:22

Enrichment of Bruch's Membrane from Human Donor Eyes

Published on: November 15, 2015

12.6K
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

31.3K

Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • Atypical hemolytic uremic syndrome (aHUS) is a severe kidney disease caused by complement pathway dysregulation.
  • Autoantibodies targeting complement factor H (FH) are a significant factor in pediatric aHUS cases.
  • These autoantibodies are often linked to genetic deletions in FH-related proteins FHR1 and FHR3.

Purpose of the Study:

  • To investigate the role of anti-FH autoantibodies in aHUS pathogenesis.
  • To understand the relationship between autoantibody levels and disease activity.
  • To evaluate treatment strategies for aHUS associated with anti-FH autoantibodies.

Main Methods:

  • Analysis of autoantibody levels in aHUS patients at disease onset and during relapse.
  • Correlation of autoantibody levels with FH functional deficiency.
  • Assessment of treatment responses (plasma exchange, immunosuppression) in relation to autoantibody decline.

Main Results:

  • High anti-FH autoantibody levels correlate with aHUS onset and relapses, causing functional FH deficiency.
  • Declining autoantibody levels, achieved through plasma exchange and immunosuppression, are associated with disease remission.
  • Anti-FH autoantibodies are also found in some C3 glomerulopathy patients.

Conclusions:

  • Autoantibodies against FH are a key driver of aHUS in a subset of patients.
  • Therapeutic strategies targeting these autoantibodies, such as plasma exchange and immunosuppression, are effective for remission.
  • Understanding anti-FH autoantibodies is crucial for managing aHUS and potentially C3 glomerulopathies.