T-cell and B-cell immunity in celiac disease

Best Pract Res Clin Gastroenterol. 2015 Jun;29(3):413-23. doi: 10.1016/j.bpg.2015.04.001. Epub 2015 May 7.

Abstract

Celiac disease is an inflammatory disorder with leukocyte infiltration and changes of tissue architecture of the small intestine. The condition develops in genetically susceptible individuals as the result of an inappropriate immune response to gluten proteins of wheat, barley and rye. The clinical manifestations and the histological changes normalize when gluten is eliminated from the diet. CD4(+) T cells that recognize gluten peptides bound to predisposing HLA-DQ molecules play a key role in the pathogenesis. These T cells recognize better gluten peptides that are deamidated, and this posttranslational modification is mediated by the enzyme transglutaminase 2 (TG2). Another hallmark of celiac disease is the production of antibodies to gluten as well as to TG2. A role for B cells in celiac disease pathogenesis is receiving increased recognition. This review will discuss the main discoveries in the field of T-cell and B-cell biology of celiac disease.

Keywords: Antibody; B cell; Celiac disease; Deamidation; Epitope; Gluten; HLA-DQ2; HLA-DQ8; T cell; Transglutaminase-2.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Autoantibodies / immunology
  • Autoantigens / immunology
  • B-Lymphocytes / immunology*
  • Celiac Disease / immunology*
  • GTP-Binding Proteins / immunology
  • Glutens / immunology
  • Humans
  • Protein Glutamine gamma Glutamyltransferase 2
  • T-Lymphocytes / immunology*
  • Transglutaminases / immunology

Substances

  • Autoantibodies
  • Autoantigens
  • Glutens
  • Protein Glutamine gamma Glutamyltransferase 2
  • Transglutaminases
  • GTP-Binding Proteins