Immunopathology of Celiac Disease

Valérie Abadie, Bana Jabri

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

2 Scopus citations

Abstract

Celiac disease (CD) is a T cell-mediated intestinal disorder induced by dietary gluten in genetically susceptible individuals. It is a prototypic example of how the interaction between predisposing genes (human leukocyte antigen (HLA) and non-HLA genes) and the environment (gluten) can lead to the development of complex inflammatory disorders. Although anti-gluten CD4+ T cells are central in all aspects of CD pathogenesis, from the loss of oral tolerance to the generation of antibodies, intraepithelial cytotoxic CD8+ T lymphocytes are indispensable to promote intestinal tissue destruction. Furthermore, posttranslational modifications mediated by tissue transglutaminase-2 appear to be key in the initiation and/or amplification of anti-gluten T cell immunity. Despite many advances in our understanding of CD pathophysiology, how distinct immunological pathways cooperate to promote the destruction of intestinal epithelial cells is not yet fully understood. Here we summarize our current knowledge on the immunobiology of CD and discuss future research perspectives.

Original languageEnglish
Title of host publicationMucosal Immunology
Subtitle of host publicationFourth Edition
PublisherElsevier Inc.
Pages1551-1572
Number of pages22
Volume2-2
ISBN (Electronic)9780124159754
ISBN (Print)9780124158474
DOIs
StatePublished - 1 Apr 2015
Externally publishedYes

Keywords

  • Celiac disease
  • Gluten
  • HLA-DQ
  • Inflammation
  • Intraepithelial lymphocytes
  • Natural killer receptors
  • Nonclassical MHC class I molecules
  • Refractory sprue
  • Tissue transglutaminase-2
  • Villous atrophy

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