Mice infected with Trichinella spiralis developed significant enteropathy, comprising villus atrophy, crypt hyperplasia, goblet cell hyperplasia and a decrease in intra-epithelial lymphocyte numbers by 10 days post-infection, when most of the parasites had been expelled from the gut. However, worm expulsion was prevented by treatment with cyclosporin A and, despite a continued parasite burden, cyclosporin A treated animals had no villus atrophy or changes in inflammatory cell numbers. These results confirm that the expulsion of T. spiralis from the mouse gut is accompanied by a significant intestinal lesion and that both of these phenomena are T-cell mediated.
PrefaceThe induction of immunological unresponsiveness by feeding soluble antigens, termed oral tolerance, has been attracting considerable attention as a potential therapy for a variety of systemic inflammatory disorders. However, the physiological role of this phenomenon is in maintaining gastrointestinal homoeostasis and preventing immunopathology in the gut. This review will discuss the mechanisms of oral tolerance in the context of the structure and function of the gut associated lymphoid tissues (GALT), outline how defects in oral tolerance can lead to immunopathology and indicate its therapeutic potential.
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