Submitted to: Coccidiosis International Conference Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 8/30/1997
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Development of a vaccine for avian coccidiosis has been hampered by lack of understanding of the various components of host immune system leading to protective immunity. From studies of various parasitic infection models in mice, it is becoming clear that complex regulation by cytokines is involved in host immunity. Furthermore, a clear understanding of the cellular dichotomy in cytokine production in mice and the availability of immunological reagents, as well as gene knock-out mice, now make in-depth immunological study in this species feasible. In this respect, the murine coccidiosis model offers an alternative system where different components of host immunity can be dissected since a wide variety of mutant mice with various immunodeficiency are available. Recent studies of coccidiosis immunity using mutant mice clearly indicate an important role of various effector mechanisms involving T lymphocytes, macrophages, NK cells and cytokines in resistance to coccidiosis. In comparative studies of coccidiosis in chickens, in vivo and in vitro studies revealed that interferon-gamma, tumor necrosis factor and transforming growth factor-beta are induced following infection with Eimeria. Furthermore, depletion studies revealed the importance of T lymphocytes expressing the CD8 and TCR2 antigens in host protective immunity to avian coccidiosis. Taken together, studies in mice and chickens are providing a better understanding of the role of effector cells and soluble factors which control immune responses to Eimeria parasites.