The lack of effect of in vivo or in vitro JES6-1 treatment in the early CD4+ T cell activation, proliferation and IFN-γ production, and consequently in the ability to control acute parasitemia, can be explained by the high expression of CD25 since IL-2 bound to JES6-1 mAb retains the ability to interact with the high-affinity IL-2R [23]. The gene discussed is IFNG; the disease is parasitic infectious disease.