Individuals with coeliac disease get sick when they eat bread or other gluten-containing food. Why? ---- Scientists in the Sollid group are studying 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.
The group runs projects focusing on:
- B cells and the auto-antibody response of coeliac disease.
- How certain variants of HLA molecules predispose to disease development.
- Characterisation of how T cells recognise gluten peptides.
- How TG2 mediated post-translational protein modification increases antigenicity.
Group leader Professor Ludvig M. Sollid Centre for Immune Regulation Department of Immunology Oslo University Hospital Rikshospitalet PO Box 4950 Nydalen NO-0424 Oslo, Norway Tel: +47 23073811 Fax: +47 23073510 E-mail: email@example.com
Link to the Sollid group home page at CIR (Center for Immune Regulation).
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