Studies have been made on humoral and cellular immune respones in mice immunized with an attenuated strain of Toxoplasma gondii. Heat-inactivated antitoxoplasma serum did not cause morphologic changes in the organisms, but did markedly influence their interactions with host cells. Toxoplasma exposed to antibody were no longer capable of entering fibroblasts or HeLa cells. They were readily engulfed by macrophages, but the antibody treatment strikingly altered the intracellular fate of the parasites leading to killing and digestion of the toxoplasmas in phagolysosomes. Addition of antitoxoplasma antibody immediately after infection of macrophages in vitro had no effect on intracellular multiplication of the organism. The division time of virulent toxoplasmas in mouse peritoneal macrophages in vitro was markedly prolonged in cells from immunized mice. During the first 2-3 mo after immunization, the macrophages harvested from the peritoneal cavity demonstrated this cellular immunity directly; thereafter exposure of the macrophages to immune lymphocytes and toxoplasma antigen, or to supernates from such an interaction was required for induction of the maximal capacity to inhibit growth of toxoplasmas. Induction of the alternation in macrophages by the lymphocyte product was detectable in 6 h and maximal at 18-24 h. Cultivation in vitro of macrophages from immunized animals for periods longer than 48 h rendered the cells nonresponsive to the immune lymphocyte-toxoplasma product. Macrophages from the peritoneal cavities of normal, nonimmunized mice were also incapable of developing the capacity to inhibit growth of toxoplasmas in response to this product. The nonresponsiveness of normal macrophages, or of macrophages cultured for several days in vitro was not changed by exposure of the cells to antitoxoplasma serum.

No abstract

The rate of pinocytosis by macrophages when measured by uptake of horseradish peroxidase was significantly reduced during toxoplasma infection of the cells in vitro when the macrophages were from toxoplasma-immune mice and when control cells were stimulated in vitro to inhibit toxoplasma multiplication. There was, however, no direct correlation between reduced pinocytosis in this model and inhibition or enhancement of toxoplasma multiplication. We conclude that a reduced pinocytic rate is a feature of the unstimulated toxoplasma-immune macrophage, but this change in rate alone does not correlate with the cell's ability to inhibit toxoplasma. In addition, we observed that enhanced pinocytosis as seen in the elicited macrophage was not a requirement for inhibition of toxoplasma multiplication.

No abstract