In parasitic diseases, eosinophilia is controlled at the systemic level by soluble, circulating factors. In addition to their medullar production and migration to tissues involved by parasitosis, eosinophil populations in inflammatory infiltrates may be locally amplified by their in situ proliferation. In granulomas induced in liver tissue by eggs of schistosome worms, eosinophil proliferation and differentiation are observed. We have shown that they were under control of two cytokines, the activity of which can be demonstrated in supernatants of isolated granulomas maintained in culture for 24 hours. One of them has been identified as interleukin-5. The other one is secreted by adherent cells obtained from periovular granulomas, among which macrophages represent more than 99% of cells. It is considered to correspond to the previously described factor, secreted by inflammatory macrophages mobilized on intraperitoneal glass implants in mice with chronic schistosomiasis. In acute schistosomiasis, the activity of the interleukin-5 was predominant, whereas in the chronic phase of the disease, the stimulation of peripheral eosinopoiesis is taken over by the factor secreted by adherent cells. During the progression from the acute to the chronic phase of schistosomiasis, the immune reactivity of the host is down-regulated by T suppressor lymphocyte circuits. In addition, a redistribution of cellular controls of the host reaction to parasites may act as a complementary mechanism for establishment of the viable equilibrium between host and parasite.