Coeliac disease

CIR studies coeliac disease to understand the interplay between genetic and environmental factors in chronic inflammatory disorders.

Gluten, genes and auto-antibodies

Individuals with coeliac disease get sick when they eat bread or other gluten-containing food. Why?

CIR scientists, mainly in the Sollid group and Qiao group, study coeliac disease as a model to understand the interplay between genetic and environmental factors in chronic inflammatory disorders.

Coeliac disease patients show strong association with particular gene variants within the human leukocyte antigen (HLA) complex, particularly HLA-DQ2 and HLA-DQ8. These HLA molecules are directly involved in the pathogenesis of coeliac disease by binding and presenting gluten peptides to disease-specific T cells in the intestines of coeliac patients.

Presence of IgA and IgG antibodies specific for the auto-antigen transglutaminase (TG)2 is an other hallmark of active coeliac disease. Conspicuously, TG2 is not only the target for auto-antibodies in coeliac disease, but it is also important for creation of antigenic gluten T-cell epitopes.

Currently scientists at CIR are trying to understand how disease specific auto-antibodies to TG2 are generated, and why auto-antibody production is dependent on HLA-DQ2 expression as well as dietary gluten exposure.

Published Feb. 7, 2012 3:26 PM - Last modified Aug. 31, 2015 2:56 PM