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Rationales behind novel therapies for coeliac disease

Ludvig Sollid

Professor Ludvig Sollid

Ludvig Sollid is the Director of the Centre for Immune Regulation, Oslo, Norway, Professor at the University of Oslo and a Senior Consultant at the Oslo University Hospital - Rikshospitalet. He has a research interest in the genetic basis of autoimmune diseases. His group has made important contributions to the understanding of the molecular basis of coeliac disease. He has been recognised for his scientific contributions by several awards, notably the Research Council of Norway's Møbius Prize for Outstanding Research (Oslo, 2006), the Warren Prize for Excellence in Coeliac Disease Research (San Diego, 2007), the Rank Prize in Nutrition (London, 2010) and the United European Gastroenterology Research Prize (Amsterdam, 2012).




Coeliac disease is a prevalent polygenic disorder caused by a harmful immune response to gluten. By far the single most genetic factor is the major histocompatibility complex and the primary association with HLA-DQ2.5, HLA-DQ2.2 and HLA-DQ8. These HLA molecules present gluten epitopes to CD4+ T cells – cells which can be considered to be the master regulators of the immune reactions leading to the disease. Gluten epitopes recognised by T cells are typically deamidated, and this deamidation is mediated by the enzyme transglutaminase 2 (TG2). Strikingly, coeliac disease patients have very disease specific autoantibodies to TG2, and these antibodies are only produced in subjects who carry the coeliac disease associated HLA molecules, when they consume gluten. It is hardly coincidental that TG2 is implicated in T cell epitope formation and being a target for autoantibodies. New evidence suggests that B cells with their surface immunoglobulin antigen receptor, both B cells specific for gluten as well as TG2, serve as antigen presenting cells for gluten reactive T cells thereby amplifying the T cell response. The insights into the key pathogenic events offer interesting targets for therapy. Many of the explored targets centre around the gluten reactive CD4+ T cells, ranging from reducing the gluten antigen exposure to modulating the T cell effector functions. The assessment of therapeutic intervention relies on good surrogate markers of disease activity. The insight into the pathogenesis also points to good candidates, yet versatile, robust surrogate markers remain to be identified. Fulfilling this need should be a priority in future efforts.

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