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This paper deals with basic problems of glucocorticoid eosinopenia and of regulations within the eosinophile cell system. The effects of glucocorticoids on single regulatory factors of this system, such as eosinotactic stimuli, eosinopoiesis, life span and rate of removal of eosinophils, are discussed in detail. Eosinophilopoiesis is not influenced by glucocorticoids. This finding, added to the observation that blocking the reticuloendothelial system suppresses the glucocorticoid eosinopenia and that these compounds have no eosinolytic properties in vitro, speaks against the contention that the eosinopenic effect of the glucocorticoids is actually due to a direct lytic effect on the eosinophils. A distributional shift of eosinophils in vascular sectors functioning as blood depots, or a migration into tissues can be abandoned as explanations of glucocorticoid eosinopenia. The hypothesis of a fixation at sites of physiologic demand is certainly not a valid explanation of glucocorticoid eosinopenia, since glucocorticoids suppress the eosinotactic stimuli. Blocking experiments of the RES show that the rate of disappearance of the eosinophils is a resultant of the functional condition of the RES and of the sum of the eosinopenic stimuli. On the basis of our investigations we arrive at the conclusion that glucocorticoid eosinopenia depends upon an inhibition of the release of mature eosinophils from the bone marrow and upon an increased destruction of eosinophils in the reticuloendothelial system. The level of the original eosinophilia, that is to say, the percentage of young forms with a long life expectancy, determines the degree of eosinopenia attained by a single application of glucocorticoid and the time lapse before aneosinophilia develops under continuous glucocorticoid administration.

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