Cell-Mediated Immunity Against Besnoitia and Toxoplasma in Specifically and Cross-Immunized Hamsters and in Cultures

Abstract

The capacity of hamster peritoneal cell populations to control viability and growth of Besnoitia and Toxoplasma organisms was assessed in vivo and in vitro. Immunized hamsters reduced the homologous organisms 100- to 10,000-fold over a 5-day period, but the heterologous infection increased 100- to 1,000-fold in numbers, similar as in the nonimmune controls. Passively administered antibody was ineffective although lytic cofactors were supplied by hamsters. In cultures, peritoneal cells from Besnoitia-immune hamsters delayed the growth of homologous parasites to an average of 38.5 h per division; however, in Toxoplasma-immune and nonimmune cells, Besnoitia divided every 12.8 h. Specificity of immunity was pronounced against both infections. With cross-infections, Toxoplasma-immune cultures did not effectively delay Besnoitia growth; however, Besnoitia-immune cultures reduced Toxoplasma growth by one-half. Co-cultivation experiments demonstrated that specifically committed lymphocytes could instruct macrophages to reduce the homologous organism 10-fold, whereas heterologous organisms were reduced only 2-fold. Lymphocyte supernatants initiated hypersensitivity as indicated by macrophage activation and giant cell formation in culture. However, these supernatants did not transfer infection immunity. Lymphokines could account for the hypersensitivity phenomena, but cell-mediated infection immunity in this model required close lymphocyte-macrophage proximity. These studies indicate that a number of distinct processes including delayed hypersensitivity, macrophage activation, and specific cellular immunity are acting simultaneously during latent Besnoitia infection of hamsters. All three processes are mediated by lymphoid cells and appear to be specifically induced. Although activated macrophages develop some heightened nonspecific capabilities, these were several orders of magnitude below the specific effects.

Production and Properties of Immune Interferon from Spleen Cell Cultures of Toxoplasma‐Infected Mice

“…However, the mechanism whereby the cells acquire the enhanced ability to inhibit or kill this parasite is still unclear . Several studies with experimental animal and human models have shown that nonimmune macrophages cocultured with lymphocytes from Toxoplasma-immune hosts and specific antigen can acquire anti-Toxoplasma activity (9,22). Based on these findings, a number of attempts have been made to induce anti-Toxoplasma activity within nonimmune macrophages or human monocytes by incubation with supernatants obtained from specifically stimulated immune lymphocytes (2,4,21,22).…”

ACTIVATED MOUSE MACROPHAGES: MORPHOLOGY, LYSOSOMAL BIOCHEMISTRY, AND MICROBICIDAL PROPERTIES OF IN VIVO AND IN VITRO ACTIVATED CELLS

“…This applies equally well to L. monocytogenes as to T . gondii infections (10,14,21,24). The ultimate killer cells in these infections are the activated macrophages (20,23,25,34).…”

Toxoplasma gondii: its effect on the ovine popliteal lymph node

“…Humoral antibody by itself is not considered to be of primary importance (Lindberg and Frenkel, 1977) because cell-mediated mechanisms have been shown to play the principal role in uitro (Remington, Krahenbuhl and Mendenhall, 1972;Borges and Johnson, 1975;Jones, Len and Hirsch, 1975), and in uiuo (Frenkel, 1967;Hoff and Frenkel, 1974). Furthermore, the thymus plays an essential part in the development of immunity to T. gondii (Hof et al, 1976;Buxton, 1980).…”