|JAKOWLEW, SONIA - NATIONAL CANCER INST
Submitted to: Handbook of Vertebrate Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/1/1996
Publication Date: N/A
Interpretive Summary: Avian coccidiosis is a major parasitic disease of poultry which causes greater than $600 million annual loss to poultry industry. The ability to vaccinate chickens against coccidiosis will have a major impact on industry. Development of an immunological strategy is one of the major goals of ARS coccidiosis research. To understand better host immune response to coccidian parasites, ARS scientist, in collaboration with a scientist a National Cancer Institute, examined various intestinal immune cells. The results indicate that intestinal lymphocytes mediate immune response to parasites by secreting soluble hormone-like factors which have effect on parasites survival. Understanding how host immune cells are stimulated to produce such hormone-like factors to kill parasites will lead to new immunological control strategies for intestinal diseases of chickens.
Technical Abstract: Intestinal immune responses to microbial pathogens that lead to protective immunity involve the complex interplay of soluble factors, leukocytes, epithelial cells, endothelial cells, and other physiological factors of the gut-associated lymphoid tissues (GALT). The research on immunity to coccidiosis demonstrates that immune responses to these parasites are extremely complex. Different effector mechanisms may be involved depending on the response is occurring. It will undoubtedly be some time before a detailed description of immune mechanisms involved in protection against coccidiosis becomes clear. It is likely that these complex interactions have contributed to the difficulties in developing an effective vaccine against Eimeria spp. However, recent technical advances in molecular and cellular immunology have facilitated our understanding of the ontogeny, structure, and function of the GALT and led to investigations of the roles of intestinal lymphocyte subpopulation in coccidia disease processes.