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Genes and environment in celiac disease.

L M Sollid1, S N McAdam, O Molberg

  • 1Institute of Immunology and Medical Department, Rikshospitalet, University of Oslo, Norway. l.m.sollid@labmed.uio.no

Acta Odontologica Scandinavica
|August 15, 2001
PubMed
Summary

Celiac disease involves genetic and environmental factors, with HLA genes like DQ2/DQ8 playing a key role. The immune response to gluten, mediated by T cells and tissue transglutaminase, is critical for disease development.

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Area of Science:

  • Immunology
  • Genetics
  • Gastroenterology

Background:

  • Celiac disease is an intestinal disorder influenced by genetic and environmental factors.
  • While HLA genes are major predisposing factors, non-HLA genes also contribute modestly.
  • Previous studies indicate CTLA4 or nearby genes are among these non-HLA contributors.

Purpose of the Study:

  • To investigate the role of HLA-DQ2 and HLA-DQ8 in presenting gluten peptides to T cells in celiac disease.
  • To explore the mechanism of gluten peptide modification and presentation in the context of celiac disease.

Main Methods:

  • Isolation of gluten-reactive CD4+ T cells from small intestinal biopsies of celiac patients.
  • Analysis of HLA molecule binding to deamidated gluten epitopes.

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  • Investigation of the role of tissue transglutaminase (tTG) in gluten peptide modification.

    • Main Results:

    • Gluten-reactive T cells were found in celiac patients but not controls.
    • HLA-DQ2 and HLA-DQ8 molecules present specific gluten peptides to T cells.
    • Deamidation of gluten epitopes by tTG creates residues that bind effectively to DQ2/DQ8.

    Conclusions:

    • The immune response to gluten, controlled by intestinal T cells restricted by HLA-DQ2 or HLA-DQ8, is a critical checkpoint for celiac disease.
    • HLA's dominant genetic role is explained by this immune checkpoint.
    • Non-HLA genes may influence lesion formation pathways, potentially with less critical checkpoints.