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

Experimental IgA nephropathy induced by oral immunization.

S N Emancipator, G R Gallo, M E Lamm

    The Journal of Experimental Medicine
    |February 1, 1983
    PubMed
    Summary

    Oral immunization in mice induced a specific IgA antibody response, leading to IgA deposition in the kidneys. This experimental model mimics key features of human IgA nephropathy.

    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

    T cell cytokine polarity as a determinant of immunoglobulin A (IgA) glycosylation and the severity of experimental IgA nephropathy.

    Clinical and experimental immunology·2008
    Same author

    Animal models of IgA nephropathy.

    Current protocols in immunology·2008
    Same author

    The role of nasal tolerance in a model of IgA nephropathy induced in mice by Sendai virus.

    Clinical immunology (Orlando, Fla.)·2004
    Same author

    T cell cytokines determine the severity of experimental IgA nephropathy by regulating IgA glycosylation.

    Clinical and experimental immunology·2001
    Same author

    Tissue distribution of products of the mouse decay-accelerating factor (DAF) genes. Exploitation of a Daf1 knock-out mouse and site-specific monoclonal antibodies.

    Immunology·2001
    Same author

    Treatment of collagen induced arthritis by proteolytic enzymes: immunomodulatory and disease modifying effects.

    The Journal of rheumatology·2001

    Area of Science:

    • Immunology
    • Nephrology
    • Gastroenterology

    Background:

    • IgA nephropathy (IGAN) is a primary glomerular disease.
    • The pathogenesis of IgAN remains incompletely understood.
    • A potential link between mucosal immunity and IgAN has been hypothesized.

    Purpose of the Study:

    • To investigate if a mucosal immune response can induce IgA nephropathy.
    • To establish an experimental model for IgAN.

    Main Methods:

    • Mice were orally immunized with protein antigens for 14 weeks.
    • Humoral and mucosal immune responses were analyzed.
    • Kidney tissues were examined for IgA, immunogen deposition, and ultrastructural changes.

    Main Results:

    • Oral immunization resulted in a specific IgA antibody response.
    • Deposits of IgA and immunogen were found in the glomerular mesangium of immunized mice.
    • Ultrastructural analysis revealed electron-dense mesangial deposits, characteristic of IgAN.

    Conclusions:

    • Mucosal immunization can trigger an immune response leading to IgA deposition in the kidneys.
    • This experimental model closely resembles the human disease IgA nephropathy.
    • Findings support the hypothesis that IgAN can arise from mucosal immune responses.

    Related Experiment Videos