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

Single nucleotide polymorphisms as a prerequisite for autoantigens.

Michael B Stadler1, Diana Arnold, Sara Frieden

  • 1Institute of Immunology, University of Bern, Bern, Switzerland. stadler@mit.edu

European Journal of Immunology
|January 4, 2005
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

Multiscale integration of tissue and chromatin context converts cell heterogeneity into stable intestinal patterning.

Cell·2026
Same author

Polycomb chromatin topology enables long-range enhancer recruitment during craniofacial development.

Nature communications·2026
Same author

The human BAF chromatin remodeler processes nucleosomes bound by pioneer transcription factors OCT4-SOX2.

Molecular cell·2026
Same author

Preventing CpG hypermethylation in oocytes safeguards mouse development.

Developmental cell·2025
Same author

The chimeric aptamer axl-miR-214sponge inhibits breast cancer and melanoma dissemination.

Molecular therapy : the journal of the American Society of Gene Therapy·2025
Same author

The histone H3 lysine 36 demethylase KDM2A/FBXL11 controls Polycomb-mediated gene repression and germ cell development in male mice.

Nature communications·2025
Same journal

Fast Generation of F(Ab')<sub>2</sub> Fragments From Human IgG Using Fc-Fused IgG-Degrading Enzyme.

European journal of immunology·2026
Same journal

Generation of Regulatory T Cells Against Islet Neoantigen.

European journal of immunology·2026
Same journal

Complement Inhibition in the Clinic: Are We Doing Enough to Protect Patients From Infection?

European journal of immunology·2026
Same journal

Special Issue: yEFIS 3rd Symposium.

European journal of immunology·2026
Same journal

CRISPR/Cas9-Mediated Gene Knockout Reveals a Nonredundant Role for p16<sup>INK4A</sup> in Controlling TCR-Dependent and Independent CD8 T Cell Expansion.

European journal of immunology·2026
Same journal

Induction of Humoral and Cellular Immunity After SARS-CoV-2 JN.1 Vaccination in Individuals With and Without Prior Infection.

European journal of immunology·2026
See all related articles

Genetic variations called single nucleotide polymorphisms (SNPs) in self-proteins may explain why the immune system attacks the body. These genetic alterations in autoantigens could be a key trigger for autoimmune diseases.

Area of Science:

  • Immunology
  • Genetics
  • Autoimmunity

Background:

  • The precise triggers for autoimmune responses, where the immune system mistakenly targets the body's own proteins (self-proteins), remain unclear.
  • A leading hypothesis suggests that only modified or altered self-proteins become targets for immune attack.

Purpose of the Study:

  • To investigate whether genetic polymorphisms, specifically single nucleotide polymorphisms (SNPs), represent the alterations that can lead to self-proteins becoming targets in autoimmune diseases.
  • To analyze sequence variability in known human autoantigens to identify potential genetic predispositions to autoimmunity.

Main Methods:

  • Comparative analysis of gene sequences.
  • Identification and quantification of single nucleotide polymorphisms (SNPs) in known human autoantigens.

Related Experiment Videos

  • Comparison of SNP frequency in autoantigens versus other human genes.

    • Main Results:

    • Autoantigens were found to contain a significantly higher number of single nucleotide polymorphisms (SNPs) compared to other human genes.
    • This increased genetic variability in autoantigens suggests a potential mechanism for immune system recognition and attack.

    Conclusions:

    • Single nucleotide polymorphisms (SNPs) in self-proteins may be a crucial factor in the initial induction of autoimmune responses.
    • These genetic alterations could explain how self-proteins become targets, potentially through allogeneic exposure and subsequent immune recognition.
    • SNPs represent a significant prerequisite for autoimmunity, alongside other contributing factors.