Infection and allergy in the small intestine are often associated with changes in mucosal architecture, usually villous atrophy and crypt hypertrophy. There is good evidence from epithelial cell kinetic studies to suggest that these morphological changes represent an adaptive response of the intestine to increased rates of epithelial cell loss and production, but the mechanisms involved are not understood. Accompanying these mucosal changes there is usually an increase in the intestinal lymphoid populations, suggesting that in addition to any non-specific toxic effects, immunological components may be involved. The purpose of this thesis is to investigate the effects of delayed hypersensitivity on mucosal architecture and lymphoid cell infiltrate. Two separate lines of research were pursued; firstly, intestine undergoing a cell-mediated rejection process was studied, and secondly, the amount of antigen present in the gut was altered by the use of antigen-free grafts, an antigen-free diet, and parasite infection.