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ARS Home » Research » Publications at this Location » Publication #68412


item Trout, James
item Lillehoj, Hyun

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/2/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Coccidiosis is an intestinal parasite disease which is caused by several different species of Eimeria. Coccidiosis results in a severe body weight loss and poor performance. A vaccine is not currently available. An alternative control strategy is urgently needed. In this paper ARS scientists studied chicken immunity to coccidiosis to determine the nature of effector cells responsible for protection of chickens against coccidiosis. Results suggest that cytotoxic host lymphocytes expressing CD8 antigen is an important effector cell. Understanding the nature of the interaction between host and parasite will lead to development of coccidial vaccine.

Technical Abstract: This study evaluated the effects of selective depletion of T lymphocytes on Eimeria infections in chickens. Cell depletions were initiated in day- or week-old Hyline SC strain chickens using intra-peritoneal injections of monoclonal antibodies to CD4, CD8, or TCR alpha/beta. Control chickens received injections of irrelevant monoclonal antibody or PBS. Following the establishment of cell depletion, chickens were infected orally with E. acervulina or E. tenella, 1x10 4 oocysts for primary infections and 2x10 5 oocysts for secondary infections. Chickens treated with anti-CD4 monoclonal antibody produced significantly more oocysts than controls following primary E. tenella but not E. acervulina infections. Development of resistance to challenge infection was unaffected. These results suggest that CD4+ lymphocytes are important in controlling primary infection with E. tenella. Chickens treated anti-CD8 or anti-TCR alpha/beta monoclonal antibodies produced significantly fewer oocysts than controls following primary infection but significantly more oocysts than controls following secondary infection with both E. tenella and E. acervulina. Additionally, anti-CD8 treatment abrogated resistance to challenge infection. CD8-depleted chickens may exhibit decreased oocyst production following primary infection due to lack of CD8+ lymphocytes to serve as transporting cells for sporozoites. The abrogation of resistance to secondary infection in CD8- and TCR alpha/beta-depleted chickens suggests that these cells are necessary for the development of protective immunity to coccidia.