To explore a possible mechanism of pregnancy-associated suppression of

The lymphokine production by pregnant mice infected with a lethal dose of Toxoplasma gondii was evaluated in comparison with that by virgin mice infected with a sublethal dose of this protozoan parasite. Splenocytes taken from mice before and on the day after infection produced considerable amounts of IL‐2 in response to concanavalin A (Con A) stimulation, but the titers rapidly declined in both pregnant and virgin mice as infection progressed. A trace amount or undetectable level of IL‐2 was produced by splenocytes from acutely infected mice when stimulated with Toxoplasma lysate antigen (TLA). In contrast to the kinetics of IL‐2 production, the levels of IFN‐γ produced by splenocytes cultured with Con A or TLA increased steadily in the later stage of infection in both pregnant and virgin mice. Thus, the response to Con A or TLA of splenocytes to produce IL‐2 and IFN‐γ differed strikingly in acute toxoplasmosis in mice. The administration of rHuIL‐2 resulted in a significant decrease in the mortality of pregnant mice infected with a lethal dose of Toxoplasma. The combination of rHuIL‐2 and rMuIFN‐γ increased the survival rate slightly but not significantly compared with pregnant mice receiving either rHuIL‐2 or rMuIFN‐γ. Moreover, exogenously administered rHuIL‐2 enhanced the production of both IFN‐α and IFN‐γ in the bloodstreams of pregnant mice, in accordance with the decreased mortality. These results indicate that IL‐2 may play a significant role in modulating the host defense against Toxoplasma infection in pregnant mice.