Natural regulatory T cells constitutively express the IL-2Rα chain (CD25) on their surface. Consequently, administration of anti-CD25 antibodies is a commonly utilized technique to deplete regulatory T cell populations in vivo. However, activated effector T cells may also transiently express CD25, and are thus also potential targets for anti-CD25 antibodies. In this study utilizing Toxoplasma gondii as a model pro-inflammatory infection we have examined the capacity of anti-CD25 antibodies to target effector T cell populations during an inflammatory episode, to determine to what extent that this may modulate the outcome of disease. Anti-CD25 antibody treated C57BL/6 mice displayed significantly reduced CD4+ T cell IFN-γ production during acute T. gondii infection and exhibited reduced weight loss and liver pathology during early acute infection; aspects of infection previously associated with effector CD4+ T cell responses. In agreement, anti-CD25 antibody administration impaired parasite control and caused mice to succumb to infection during late acute/early chronic stages of infection with elevated tissue parasite burdens. In contrast, anti-CD25 antibody treatment of mice with established chronic infections did not markedly affect brain parasite burdens, suggesting that protective T cell populations do not express CD25 during chronic stages of T. gondii infection. In summary, we have demonstrated that anti-CD25 antibodies may directly abrogate effector T cell responses during an inflammatory episode, highlighting important limitations of the use of anti-CD25 antibody administration to examine regulatory T cell function during inflammatory settings.