Letter to the Editor

摘要

Dear Sir,In issue 41, Alaedini and Green provided a review of autoantibodies in celiac disease . In particular, they considered anti-transglutaminase 2 (TG2) antibodies, directed against the autoantigen tissue TG and whether these antibodies may play a role in the pathogenesis of celiac disease. The authors conclude "the available evidence suggests that they (the antibodies) have the potential to have a pathogenic contribution". For the reasons outlined below, I believe that, instead, the available evidence provides little support for this view.Firstly, Alaedini and Green cite research showing that anti-TG2 antibodies interfere with the bioactivity of the TG enzyme and thus may detrimentally affect its role in cell differentiation through reducing its catalysing ability . However, this is not well-proven and other studies have shown that when bound by anti-TG2 antibodies, the TG2 enzyme retains a significant level of residual activity and allows catalysis to occur .Indeed, the immunogenic epitopes of TG2 that the autoantibodies bind to have been identified and do not include the active site . Instead, the antibodies were directed against domains in the N and C terminal regions. Furthermore, the notion of anti-TG2 antibodies inhibiting the enzyme is contrary to the proven role of TG in bringing about the celiac immune reaction through deamidation of gliadin.