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 activation in experimental IgA nephropathy: an antigen-mediated process.

A Rifai1, A Chen, H Imai

  • 1Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, Houston.

Kidney International
|December 1, 1987
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

Observation of a Charmed Baryon Decaying to D;{0}p at a Mass Near 2.94 GeV/c;{2}.

Physical review letters·2007
Same author

Observation of CP violation in B --> eta'K0 decays.

Physical review letters·2007
Same author

Observation of time-dependent CP violation in B0 --> eta'K0 decays and improved measurements of CP asymmetries in B0 --> phiK0, KS0KS0KS0 and B0 --> J/psiK0 decays.

Physical review letters·2007
Same author

Vector-tensor and vector-vector decay amplitude analysis of B0-->phiK*0.

Physical review letters·2007
Same author

Observation of B-->eta'K* and evidence for B+-->eta'rho+.

Physical review letters·2007
Same author

Measurement of the CP asymmetry and branching fraction of B0-->rho0K0.

Physical review letters·2007
Same journal

KDIGO Life Cycle of Guideline Development Series Part 6: Bridging the Gap between Guidelines and Clinical Practice: The KDIGO Approach to Global Implementation and Education in Nephrology.

Kidney international·2026
Same journal

KDIGO Life Cycle of Guideline Development Series Part 5: Guideline updates and a living model for the future.

Kidney international·2026
Same journal

Crystal-storing histiocytosis causing severe acute kidney injury.

Kidney international·2026
Same journal

Peritoneal dialysis in a patient with extensive burn scarring.

Kidney international·2026
Same journal

COPA syndrome unmasked by anti-neutrophil cytoplasmic antibody-positive immune-complex nephritis.

Kidney international·2026
Same journal

Monitoring anti-nephrin antibodies in the management of recurrent diffuse podocytopathy.

Kidney international·2026
See all related articles

The presence of specific antigens is crucial for activating complement within IgA immune deposits, preventing kidney injury. This research clarifies how antigen-specific IgA immune complexes trigger complement, a key factor in renal disease.

Area of Science:

  • Immunology
  • Nephrology

Background:

  • Complement activation via immune complex glomerular deposition contributes significantly to renal injury.
  • Understanding the mechanisms by which IgA immune complexes activate complement is vital for addressing kidney damage.

Purpose of the Study:

  • To investigate whether the presence of an antigen within glomerular IgA immune deposits is necessary for complement activation.
  • To elucidate the role of antigen structure in IgA-mediated complement activation and subsequent renal injury.

Main Methods:

  • Experiments involved administering cross-linked IgA oligomers (X-IgA) with and without specific antigens to mice.
  • Immunofluorescence microscopy was used to detect glomerular IgA and C3 deposits.
  • Pre-formed IgA immune complexes with varying antigenic features were utilized to assess complement activation.

Related Experiment Videos

Main Results:

  • Glomerular C3 deposits, indicating complement activation, were only observed when antigens were bound to X-IgA.
  • IgA deposits were equivalent in intensity and pattern, but C3 deposition was exclusively linked to immune complexes containing a specific antigenic modification (DNP).
  • Complement C3 conversion to iC3b by IgA immune complexes was highly dependent on the nature of the antigen.

Conclusions:

  • The antigen's presence and specific structural features within IgA immune deposits are essential for initiating complement activation.
  • These findings highlight the critical role of antigen-specific IgA immune complexes in driving complement-mediated renal pathology.