Intestinal inflammation results from derangement of those mechanisms of innate and acquired immunity which subtly regulate the local immune response.1 This is the case in Crohn's disease and coeliac disease, both characterised by marked mucosal lymphocyte infiltration, abnormal T cell activation, and upregulation of Th1 cytokines.2

In recent years another piece has been added to the entangled puzzle of intestinal inflammation. Apoptosis, a highly controlled process of cell death,3 modulates immune and inflammatory responses by limiting expansion of activated T lymphocytes and deleting autoreactive T cell clones.4 ,5 At the intestinal mucosal level, this process may be of particular relevance ensuring that physiological lamina propria T cell activation, due to chronic exposure to dietary antigens and exogenous pathogens, does not result in inflammatory tissue damage. Otherwise, defective T cell apoptosis may lead to a state of uncontrolled intestinal inflammation, and has been reported in coeliac disease6 and in Crohn's disease.7 ,8In the former, decreased lymphocyte apoptosis has been found at the level of the epithelial compartment,6 and this defect, favouring expansion of intraepithelial lymphocytes with an abnormal phenotype and a restricted repertoire, may precede the onset of refractory sprue9 or T cell lymphoma.10Unlike …