Celiac disease as a model for SLE

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Celiac disease as a model for SLE Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). Celiac disease as a model for SLE. In celiac disease, both the trigger (gluten) and drivers (activated T and B memory cells) lead to production of autoantibodies (in this case targeted to transglutaminase 2) (left panel). If the offending external antigen is removed, the disease goes into remission but persistence of memory T and B cells renders patients exquisitely sensitive to exacerbations of disease upon re-exposure to antigen. In SLE (right panel) the dominant site of antigenic stimulation is proposed to be skin rather than gut. Here, UV light acts as the trigger. In contrast to cytotoxic CD8 T cells in celiac, the key driver in SLE is memory B cells but T cells may also play a role. (Figure modified from Ludvig et al. Nat Rev Immunol 2013;13:294–303)‏ Jill P Buyon et al. Lupus Sci Med 2015;2:e000087 ©2015 by Lupus Foundation of America