Hindawi Publishing Corporation Journal of Biomedicine and Biotechnology Volume 2010, Article ID 786078, 9 pages doi:10.1155/2010/786078 Research Article Reduction of Foxp3 + Cells by Depletion with the PC61 mAb Induces Mortality in Resistant BALB/c Mice Infected with Toxoplasma gondii Eda Patricia Tenorio, Jonadab Efra´ ın Olgu´ ın, Jacquelina Fern ´ andez, Pablo Vieyra, and Rafael Saavedra Departamento de Inmunolog´ ıa, Instituto de Investigaciones Biom´ edicas, Universidad Nacional Aut´ onoma de M´ exico, Apartado Postal 70228, C.U., CP 04510, Mexico City, Mexico Correspondence should be addressed to Rafael Saavedra, saavedra@servidor.unam.mx Received 30 June 2009; Revised 9 September 2009; Accepted 14 September 2009 Academic Editor: Luis I. Terrazas Copyright © 2010 Eda Patricia Tenorio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Regulatory T cells (Tregs) are CD4 + Foxp3 + cells that modulate autoimmune responses. Tregs have been shown to be also involved during the immune response against infectious agents. The aim of this work is to study the role of Tregs during the infection with the intracellular protozoan Toxoplasma gondii. Resistant BALB/c mice were injected with 200 μg of anti-CD25 mAb (clone PC61) and 2 days later they were infected with 20 cysts of the ME49 strain of T. gondii. We observed that depleted mice showed 50–60% mortality during the acute infection. When FACS analysis was carried out, we observed that although injection of PC61 mAb eliminated 50% of Tregs, infected-depleted mice showed a similar percentage of CD25 + Foxp3 − (activated T cells, Tact) to those observed in infected nondepleted animals, demonstrating that in our depletion/infection system, injection of PC61 mAb did not hamper T cell activation while percentage of Tregs was reduced by 75% 10 days post infection. We concluded that Tregs are essential during protection in the acute phase of T. gondii infection. 1. Introduction Toxoplasma gondii (T. gondii) is an intracellular parasite and the etiological agent of toxoplasmosis. Although the infection is asymptomatic in most immunocompetent indi- viduals, toxoplasmosis may cause severe complications in immunocompromised individuals [1, 2]. If T. gondii infec- tion occurs during pregnancy, transplacental transmission can occur, leading to abortion or congenital malformations [2–5]. The immune response against T. gondii has been largely characterized and it has been demonstrated that cell medi- ated immunity is essential to control infection [2, 6, 7], involving synergy between CD4 + and CD8 + T cells [8, 9]. T. gondii triggers the production of IL-12, mainly by dendritic cells [10–12], which stimulate NK cells and T lymphocytes to secrete large amounts of IFN-γ, a key cytokine for protection against this parasite [10, 13, 14]. Thus, protection against T. gondii is dependent on a TH1 response [15]. However IL- 10 is also required for prevention of development of IFN-γ mediated pathology [16]. Regulatory T cells (Tregs) are a subset of CD4 + T cells that control the immune response by suppressing many lymphocyte effector functions [17–19]. Natural Tregs consti- tutively express CD25 (the α chain of the IL-2 receptor) [20], CTLA-4 [21], and the forkhead family transcription factor Foxp3 [22, 23], which is required for their development and function [22]. Although initially described for preventing autoimmune responses [20, 24, 25], it has also been demon- strated that they can regulate the immune response against infectious agents [26–29]. For example, in vivo depletion of CD25 + cells leads to an increase in the production of IFN-γ in animals infected with Plasmodium chabaudi adami [30] and Trypanosoma congolense [31], or in animals infected with Schistosoma mansoni to an increased production of IFN-γ, IL-4, IL-5, and IL-13 [32], indicating that Tregs can