In response to antigenic stimulation, spleen cells from Toxoplasmainfected mice produce a factor showing inhibitory activity against vesicular stomatitis virus infection in L cell cultures. When BALB/C and ICR mice were inoculated intraperitoneally with the low-virulent S-273 strain of T. gondii, such activity was first detected in 4 and 7 days and reached maximum levels at 10 and 14 days respectively, and retained these levels for at least three weeks. However, BALB/C mice, which are considerably more sensitive to Toxoplasma infection than ICR mice, produced significantly smaller amounts of interferon (IF) after challenge with the high virulent strain.The IF produced in this system possessed certain known properties of immune (type II) IF and was not neutralized by rabbit antiserum against mouse type I IF. The immune IF preparation also inhibited multiplication of Toxoplasma within nonphagocytic L cells in an IF-like fashion, whereas Newcastle disease virusinduced (type I) IF had no effect on this parasite. The antiviral and anti-Toxoplasma activity in immune IF preparations could not be distinguished solely on the bases of their molecular weight and isoelectric point. The experiments with anti-0 serum plus complement and with nylon wool column effluent cells strongly suggest that immune IF was produced by T lymphocytes and required the assistance of macrophages.
In vitro assessments were carried out to study some biological aspects of immune lymphocytes producing a new lymphokine, called by the authors Toxoplasma growth inhibitory factor (Toxo-GIF), which inhibits the intracellular multiplication of Toxoplasma gondii within nonimmune mouse macrophages. Concanavalin A and phytohemagglutinin-P were found to induce vigorous production of Toxo-GIF, whereas bacterial lipopolysaccharide did not. In vitro treatment of splenic lymphocytes with rabbit anti-mouse thymocyte serum plus complement abolished almost completely their ability to produce Toxo-GIF. Treatment of splenic lymphocytes with inhibitors of protein synthesis, cycloheximide or puromycin resulted in a remarkable reduction of the ability of sensitized lymphocytes to produce this lymphokine. Thus the production of Toxo-GIF seems to be dependent on the cellular metabolic events of sensitized T-lymphocytes. The significant activity of Toxo-GIF was demonstrable even in the supernate of lymphocyte cultures incubated in serum-free medium and was also evident after immune lymphocytes and homologous antigen were incubated for the relatively short period of 10 h.
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