In order to understand the mechanisms involved in adverse reactions to food proteins which are mediated by the immune system it is necessary to understand the normal immune response following the ingestion of dietary proteins. Thus, the effect of age, source and quantity of protein species of animal and maternal influences on this response have been examined. Introduction of a novel dietary protein to the diet of mature rabbits resulted in a greater immune response compared to the weanling, indicating absorbtion of antigenic protein in sufficient quantities to stimulate the production of circulating antibodies is not only a function of the immature intestine. Production of serum specific antibodies is influenced by the duration of antigenic exposure, source and quantity of ingested protein. The magnitude of the immune response appeared to be due to the quantity of antigenic protein reaching the circulation. Specific systemic hyporesponsiveness was observed in rabbits following maternal exposure to the dietary protein. This was also influenced by the quantity of ingested protein and duration of antigenic exposure. In contrast, this treatment did not produce systemic tolerance in the mouse, instead the offspring demonstrated high levels of specific serum antibodies. The mouse differs from the rabbit and human by receiving the majority of passive immunity post-natally. Thus, the systemic immune response observed in the weanling mouse is influenced by maternal antibodies. Acute ingestion of cows milk and goats milk by human volunteers did not result in increased levels of specific circulating antigen or Clq binding immune complexes in the majority of volunteers. This suggests that the intestine provides an efficient barrier against the absorbtion of large quantities of antigenic protein in most adults. A certain amount of evidence suggests that immune mechanisms play a role in the pathogenesis of atherosclerosis; however, the immune responses in rabbits following the ingestion of a milk based diet did not influence the development of atherosclerosis.