Antigen receptors of disease-relevant T cells and B cells in celiac disease
Il 24/03/2017 ore 14.30 - 15.30
Sala Conferenze Cnr Area della Ricerca NA1, Via P. Castellino, 111 80131 Napoli
Prof. Ludvig M. Sollid from the Department of Immunology, Oslo University Hospital Rikshospitalet (Norway) will give a seminar on molecular aspects of the celiac disease.
Celiac disease is a prevalent polygenic disorder caused by a harmful immune response to gluten. By far the single most genetic factor is MHC, and the primary association is with HLA-DQ2.5, HLA-DQ2.2 and HLA-DQ8. These HLA molecules present gluten epitopes to CD4+ T cells – cells that can be considered to be the master regulators of the immune reactions leading to the disease. Gluten epitopes recognized by T cells are typically deamidated, and this deamidation is mediated by the enzyme transglutaminase 2 (TG2). Strikingly, celiac 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 the target for autoantibodies. Evidence suggests that B cells with their surface immunoglobulin antigen receptor, both cells specific for gluten and for TG2, serve as antigen presenting cells for gluten-reactive T cells thereby amplifying the anti-gluten T-cell response. Antigen receptors of disease-relevant T and B cells can be studied in detail by use of gluten/HLA-DQ tetramers and by use of labeled antigen (TG2 and gluten) that bind to surface IgA and IgM of gut plasma cells. The studies of antigen receptors provide insight of relevance for other autoimmune diseases that he will report on.
Via P. Castellino, 111 80131 Napoli
Modalità di accesso: ingresso libero