Intra-epithelial T cells in coeliac disease

In coeliac disease dietary gliadin is damaging to the small intestinal mucosa. It occurs in individuals with a genetic predisposition. In terms of pathogenesis the link between genetics and the toxic effects of gliadin remains obscure. A study in this issue of the Journal demonstrates an inherent absence of double positive CD4+CD8+ T cells in coeliac patients. It is suggested that this could result in a loss of oral tolerance and play a role in the mucosal damage of coeliac disease. In addition, it is confirmed that intra-epithelial lymphocytes are not increased in coeliac disease but there is an apparent increase due to the change in architecture, and decrease in enterocytes. Coeliac disease is an enteropathy associated with dietary gluten which occurs in individuals with a genetic predisposition. The pathogenesis remains obscure although it is clear that only certain parts of the gliadin molecule are toxic and there is considerable evidence of immunological activity, including antibody production. In this issue of European Journal of Gastroenterology and Hepatology Carton et al. present evidence in favour of an inherent depletion of CD4+CD8+ T cells, which could result in a loss of oral tolerance to ingested gliadin. Using flow cytometry they also demonstrated that the classic T-cell infiltration of coeliac disease is not due to an increase in T cells but is an apparent increase associated with a relative decrease in enterocytes as a result of the change in architecture of the mucosa. These could be important fundamental observations in helping to unravel the pathogenesis of coeliac disease.