Adoptive transfer of Treg cells to B6 mice during Toxoplasma gondii infection induces down-modulation of exacerbated inflammatory immune response but does not generate protection (MPF1P.777)

Toxoplasmosis is an infection disease affecting one third of the world population and is caused by the protozoan parasite Toxoplasma gondii . T H 1 immune response is necessary for protection, IFN-γ being the major mediator of resistance. An exacerbated T H 1 immune response however, is detrimental. Regulatory T (Treg) are CD4 + Foxp3 + cells that actively suppress pathological and physiological immune responses, thereby contributing to the maintenance of immune homeostasis. It has been reported that during acute toxoplasmosis in B6 mice, Treg cell number decreases. In order to analyze if Treg cells are involved in protection during T. gondii infection, we carried out adoptive transfer of Treg cells to infected mice. We observed a decreased mortality when Treg cells were adoptively transferred but an increased number of cysts in brain was detected. A decreased pathology in the small intestine, a decreased production of IFN-γ and TNF-α in serum, a decreased activation in CD4 + cells, and a decreased production of IFN-γ by CD4 + cells was also observed in the same mice. All these results suggest that adoptive transfer of Treg cells during T. gondii infection down-modulate the exacerbated immune response, but it does not generate protection in B6 mice. Thus Treg cells are not involved in protection during T. gondii infection.