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

The autoimmune accelerating yaa mutation does not accelerate murine AIDS.

A W Hügin1, L Fossati-Jimack, S Izui

  • 1Department of Dermatology, University Hospital, Geneva, Switzerland.

Cellular Immunology
|April 8, 2000
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

B Cell Synovitis and Clinical Phenotypes in Rheumatoid Arthritis: Relationship to Disease Stages and Drug Exposure.

Arthritis & rheumatology (Hoboken, N.J.)·2019
Same author

A lupus-susceptibility C57BL/6 locus on chromosome 3 (Sle18) contributes to autoantibody production in 129 mice.

Genes and immunity·2008
Same author

Genetic susceptibility to polyI:C-induced IFNalpha/beta-dependent accelerated disease in lupus-prone mice.

Genes and immunity·2006
Same author

Variability of the inhibition by total immunoglobulin of in vitro autoantibody-mediated erythrophagocytosis by mouse macrophages.

Clinical and experimental immunology·2006
Same author

Macrophages from patients with SLE and rheumatoid arthritis have defective adhesion in vitro, while only SLE macrophages have impaired uptake of apoptotic cells.

Annals of the rheumatic diseases·2005
Same author

Multiple loci are linked with anti-red blood cell antibody production in NZB mice -- comparison with other phenotypes implies complex modes of action.

Clinical and experimental immunology·2004

The Yaa gene does not accelerate Murine Acquired Immunodeficiency Syndrome (MAIDS). This suggests MAIDS-associated autoimmunity is secondary, with autoantibodies contributing to hypergammaglobulinemia in mice.

Area of Science:

  • Immunology
  • Genetics
  • Virology

Background:

  • Murine acquired immunodeficiency syndrome (MAIDS) exhibits lymphoproliferation, B cell activation, autoantibody production, and immunodeficiency, mirroring autoimmune diseases.
  • The Y-chromosome-linked gene, Yaa, is known to exacerbate autoimmune conditions in susceptible mouse strains.

Purpose of the Study:

  • To investigate the influence of the Yaa gene on the development and progression of Murine Acquired Immunodeficiency Syndrome (MAIDS).
  • To determine if Yaa exacerbates MAIDS, potentially linking it to autoimmune disease acceleration.

Main Methods:

  • Analysis of phenotypic and functional disease parameters in mice with and without the Yaa gene.
  • Comparative study of MAIDS progression in different genetic backgrounds.

Related Experiment Videos

Main Results:

  • The Yaa gene did not accelerate MAIDS progression.
  • This lack of acceleration is potentially due to the generalized lymphoid cell activation in MAIDS, which Yaa cannot further enhance.
  • Autoantibody production may disproportionately contribute to hypergammaglobulinemia in wild-type C57BL/6 mice with MAIDS.

Conclusions:

  • The Yaa gene does not influence the acceleration of MAIDS.
  • The autoimmune response in MAIDS appears to be a secondary phenomenon.
  • Autoantibodies play a significant role in the hypergammaglobulinemia observed in MAIDS.