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Related Experiment Videos

Autoimmunity versus tolerance: analysis using transgenic mice.

V Taneja1, C S David

  • 1Department of Immunology, Mayo Medical School, Rochester, MN 55905, USA.

Human Immunology
|February 13, 2001
PubMed
Summary
This summary is machine-generated.

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Shared epitope in rheumatoid arthritis (RA) susceptibility depends on HLA DQ and DR molecule interactions. High-affinity DR peptides may induce tolerance, while low-affinity peptides could permit autoimmunity, offering new insights into RA pathogenesis.

Area of Science:

  • Immunology
  • Rheumatology
  • Genetics

Background:

  • The shared epitope hypothesis explains the association between HLA class II alleles and rheumatoid arthritis (RA) susceptibility.
  • Complementation between HLA-DQ and HLA-DR molecules is proposed to be crucial for disease susceptibility or protection.
  • HLA-DRB1 molecules may shape the T-cell repertoire by presenting self-peptides via HLA-DQ molecules.

Purpose of the Study:

  • To test the hypothesis that HLA-DQ and HLA-DR molecule interactions influence rheumatoid arthritis (RA) association.
  • To investigate the role of peptides derived from RA-associated DR molecules in T-cell activation.
  • To determine if high-affinity DR peptides can induce tolerance and prevent autoimmune disease.

Main Methods:

  • Utilized Aβo.DQ8 transgenic mice to study collagen-induced arthritis.

Related Experiment Videos

  • Tested the ability of peptides derived from the HV3 region of RA-associated DR molecules to activate T cells.
  • Administered a peptide from the RA-resistant DRB1*0402 molecule prior to arthritis induction.

    • Main Results:

    • Peptides from RA-susceptible DR molecules showed poor binding and T-cell activation.
    • Peptides from RA-resistant DR molecules exhibited high-affinity binding and efficient T-cell activation.
    • Pre-treatment with a DRB1*0402-derived peptide prevented the onset of collagen-induced arthritis.

    Conclusions:

    • High-affinity HLA-DR-derived peptides may induce tolerance to autoimmunity.
    • Low-affinity HLA-DR-derived peptides might be permissive to autoimmunity.
    • Self-peptides derived from HLA molecules can potentially generate tolerance or autoimmunity based on their binding affinity.