Abstract

During the course of Trypanosoma cruzi infection, mice become suppressed in the ability to produce IL 2. Addition of supernatants from concanavalin A-stimulated normal spleen cells or supernatants from EL 4 cells enhanced the suppressed in vitro response of infected spleen cells to sheep erythrocytes. This enhancement was demonstrable at various times after infection and was shown not to be the result of Con A stimulation alone. Spleen cells from infected mice respond to IL 2-rich supernatants in Mishell-Dutton cultures in a dose-dependent fashion. Absorption of IL 2 activity from EL-4 supernatants by CTLL-2 cells results in a decrease in the enhancing effect of the supernatants on the in vitro antibody responses of infected spleen cells. Also, the reversal of suppression occurs only if IL 2-rich supernatants are added within 24 hr of the initiation of cultures. These results indicate that defective IL 2 production may play a role in the inability of mice infected with T. cruzi to respond appropriately to neoantigens.

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