Lines of chickens genetically selected for high (HPC)-and low-plasma corticosterone (LPC) titers were assessed for cell-mediated immunity during Marek's disease tumorigenesis. Lymphocyte transformation (using phytohemagglutinin and 2,4-dinitrofluorobenzene-bovine serum complex) and mitogen-induced cellular cytotoxicity were evaluated with peripheral blood leukocytes. Chickens from the LPC line showed a greater lymphocyte transformation response than those from the HPC line. All tumor-bearing chickens demonstrated a markedly suppressed blastogenic response. Although the blastogenic response was suppressed in those chickens infected with Marek's disease virus but not having gross tumors when compared with the steroid level, this response was greater than that of chickens with tumors and less than that of normal controls. In comparison with LPC-line chickens, HPC-line chickens demonstrated a decreased mitogen-induced cellular cytotoxicity. A decreased mitogen-induced cellular cytotoxicity was observed in both steroid lines concomitant with the onset and severity of tumors. The impaired cell-mediated response observed in the HPC line was associated with an increased tumor incidence and a greater mortality than that observed in the LPC line. Metyrapone, a chemical which blocks adrenal corticosterone synthesis, transiently enhanced mitogen-induced cellular cytotoxicity and initiated tumor regression in chickens debilitated with Marek's disease tumors.