Transamidation of gliadin mediates reversal of the antigen-specific immune phenotype in DQ8 tg mice

Celiac Disease (CD) is characterized by activation of intestinal gliadin-specific CD4+ T cells with a Th1 phenotype that plays a major role in the induction of enteropathy (1). HLA-DQ8-transgenic mice (DQ8) have widely been used to dissect the mechanisms underlying CD pathogenesis. In this model, we analysed the residual toxicity and immune response of an enzymatically modified (transamidated) gliadin (spf).