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 Experiment Videos

Complement and autoimmune glomerular diseases.

Richard J Quigg1

  • 1University of Chicago, Section of Nephrology, Chicago, Ill., USA. rquigg@medicine.uchicago.edu

Current Directions in Autoimmunity
|January 15, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Immune complex handling in transplantation: central roles for complement factor H, animal models, and translational implications.

Frontiers in immunology·2026
Same author

The complement system and kidney cancer: pathogenesis to clinical applications.

The Journal of clinical investigation·2025
Same author

The ICD-9 to ICD-10 transition has not improved identification of rapidly progressing stage 3 and stage 4 chronic kidney disease patients: a diagnostic test study.

BMC nephrology·2024
Same author

Complement: Functions, location and implications.

Immunology·2023
Same author

Macrophage Depletion Reduces Disease Pathology in Factor H-Dependent Immune Complex-Mediated Glomerulonephritis.

Journal of immunology research·2022
Same author

Local complement factor H protects kidney endothelial cell structure and function.

Kidney international·2021
Same journal

The first decade of biologic TNF antagonists in clinical practice: lessons learned, unresolved issues and future directions.

Current directions in autoimmunity·2010
Same journal

TNF in host resistance to tuberculosis infection.

Current directions in autoimmunity·2010
Same journal

TNF-alpha and obesity.

Current directions in autoimmunity·2010
Same journal

TNF and bone.

Current directions in autoimmunity·2010
Same journal

TNF-alpha: an activator of CD4+FoxP3+TNFR2+ regulatory T cells.

Current directions in autoimmunity·2010
Same journal

T cells as sources and targets of TNF: implications for immunity and autoimmunity.

Current directions in autoimmunity·2010
See all related articles

The kidney's glomerulus plays a key role in autoimmune diseases by activating the complement system. Manipulating this system offers new therapeutic strategies for glomerular diseases.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • The renal glomerulus filters plasma, but its structure predisposes it to autoimmune diseases.
  • Immune complex formation in the glomerulus activates the complement system, producing inflammatory mediators.
  • Complement activation in different glomerular regions leads to distinct pathologies: inflammatory (subendothelial/mesangial) or non-inflammatory (subepithelial).

Purpose of the Study:

  • To elucidate the role of the complement system in glomerular diseases.
  • To explore the mechanisms by which complement activation leads to glomerular injury.
  • To evaluate the therapeutic potential of modulating the complement pathway in kidney diseases.

Main Methods:

  • Utilizing genetically modified mice lacking specific complement components.

Related Experiment Videos

  • Employing antibody inhibitors and recombinant proteins targeting complement regulators.
  • Analyzing the effects of complement activation products (C3a, C5a, C3b, C5b-9) on glomerular cells and inflammation.
  • Main Results:

    • Complement activation products like C3a, C5a, and C3b trigger inflammatory responses by interacting with inflammatory cells and glomerular cells.
    • The C5b-9 membrane attack complex causes cell activation and injury, particularly in non-inflammatory settings.
    • Studies in knockout mice and with therapeutic agents have provided significant insights into complement's role in glomerular pathology.

    Conclusions:

    • The complement system is a critical mediator in the pathogenesis of glomerular diseases.
    • Targeting the complement pathway presents a promising therapeutic avenue for kidney disorders.
    • Further clinical studies are needed to confirm the efficacy of complement-modulating therapies in humans.