Cellular immunity to toxoplasma and besnoitia in hamsters: specificity and the effects of cortisol.

The inhibitory effects of cortisol on cellular immunity were studied in vitro by using hamster peritoneal exudate cells. Two obligate, intracellular protozoa--Toxoplasma gondii and Besnoitia jellisoni-- were used to control for specificity of effects. Results indicate that immune lymphocytes specifically confer immunity to (or "arm") macrophages that specifically express immunity. This arming can be inhibited by 5 microng of cortisol per ml. Macrophages that have been armed already will continue to express immunity (by limiting parasite growth specifically) in the presence of 5 microng of cortisol per ml. Cortisol levels of 20 microng/ml are required to inhibit the expression of immunity by armed macrophages. It was also found that lymphocytes, from hamsters given 20 mg of cortisol subcutaneously 2 days before the harvest of cells, did not arm macrophages, whereas macrophages from these same animals could be armed by immune lymphocytes from untreated hamsters. Therefore, it was concluded that in relation to cellular immunity, lymphocytes are more sensitive to cortisol than are macrophages. Since antibody to these parasites is almost always present in vivo, we also tested the effects of cortisol on the disposition of antibody-modified organisms by activated (not armed) macrophages, and found that 50 microng of cortisol per ml was needed to inhibit macrophage effects on antibody-treated organisms.