Regulatory T cells are involved in the maintenance of tolerance in the body and are responsible for persistence of some parasitic infections in mice like leishmaniosis and malaria. In our experiments we strived to explore the role of Treg cells in the persistence of Toxoplasma gondii infection. Outbred Swiss OFI mice were depleted of Treg cells by use of anti-CD25 monoclonal antibody during acute toxoplasmosis. No difference of mortality and brain parasitic load was observed in infected mice from depleted or non-depleted groups. In addition to CD25+ Treg cells, we observed another potential target of anti-CD25 mAb in mice acutely infected with Toxoplasma gondii. This potential target is CD25+ effector cells. A singificantly higher production ofiL-12 was also observed in mice injected with anti-CD25 mAb as compared to the control group injected with isotype control antibody. The simultaneous depletion of CD25+ Treg and CD25+ Teffector cells prohibits concluding the role of Treg cells during acute toxoplasmosis and led us to fmd another strategy to know the function of Treg cells. Swiss OFl mice were infected with type-! Toxoplasma gondii RH tachyzoites (wild type) and attenuated type-I Toxoplasma gondii Micl-3KO tachyzoites, intraperitoneally. The high expansion of CD4+CD25+Foxp3+ Treg at the local site of infection followed by expansion of CD4+CD25+ Teffector cells resulted into control of parasitemia and survival of mice infected with attenuated Micl-3KO parasites. On the other hand, the mice infected with wildtype RH parasites, died because of uncontrolled immune response and high parasitemia.