Technical Abstract: Egress, which describes the mechanism that some intracellular parasites use to exit from parasitophorous vacuoles and host cells, plays a very important role in the parasite life cycle and is central to Eimeria propagation and pathogenesis. Despite the importance of egress in the intracellular parasite’s life cycle, very little information is known on this process compared to other steps, e.g. invasion. The present study was conducted to investigate the interplay between host’s adaptive immune system and Eimeria egression. The splenic lymphocytes or soluble immune factors were incubated with parasites-infected host cells for 3 or 5 hours and the percentage of egress was calculated according to the established formula, viability of egressed parasites were tested using trypan blue exclusion and viability of host cells were tested using Annexin V and propidium iodide staining. We found that premature egression of sporozoites from E. tenella-infected primary chicken kidney cells, or from chicken peripheral blood mononuclear cells, occurred when the cells were co-cultured in vitro with spleen lymphocytes from E. tenella-infected chickens, but not when co-cultured with splenocytes from uninfected chickens. Eimeria-specific antibodies and cytokines (IFN-', IL-2, IL-15) derived from E. tenella-primed B and T lymphocytes, respectively, also were capable of promoting premature egress of sporozoite from infected host cells. Both egressed host cells and parasites were viable, although the latter with reduced re-invasion ability to some extent. These results suggest a novel, immune-mediated mechanism that the host exploites to interrupt the normal Eimeria life cycle in vivo, and thereby blocks the release of mature parasites into the environment.