Abstract
Spleen cells from inbred Fischer rats infected with Schistosoma mansoni were cultured with S. mansoni antigen, phytohemagglutinin (PHA) or concanavalin A (Con A). During the first 3 weeks of infection, both a significant proliferative response and a delayed cutaneous hypersensitivity to S. mansoni antigen were observed. In contrast, during the fourth to the seventh week both responses were reduced to a nonsignificant level, and the proliferative response to PHA or Con A also decreased during this period. At the time of minimal reactivity to PHA or Con A, the depletion of cells adherent to nylon wool (but not depletion of mononuclear phagocytic cells by plating on plastic) restored a significant response to Con A. At this time, infected rat lymphocytes reduced the proliferative response of noninfected syngeneic cells induced by Con A. This inhibition was not observed when infected cells were previously passed through a nylon wool column. Inversely, nylon wool depletion of day‐28 or 35‐infected spleen cells did not restore lymphocyte response to S. mansoni antigen. Serum (or the dialyzable fraction thereof) from day‐29‐infected rats inhibited thymidine incorporation of PHA‐stimulated normal lymphocytes and the response to S. mansoni of spleen cells from infected rats. This information suggests that at the end of the first month of infection in the rat, lymphocyte unresponsiveness to S. mansoni antigen could not be related to a demonstrable suppressor cell activity. Low molecular weight inhibitory factor(s) released by the parasite and acting directly on lymphocytes could partly account for this unresponsiveness in rat schistosomiasis.