Abstract

In this study, the role of NF-κB1 was examined during toxoplasmosis. While wildtype BALB/c mice generated protective responses, NF-κB1 −/− mice developed Toxoplasmic encephalitis, characterized by increased parasite burden and necrosis in the brain. Susceptibility was primarily associated with a local decrease in the number of CD8 + T cells and IFN-γ production, while accessory cell function appeared intact in NF-κB1 −/− mice. Consistent with these findings, T cell transfer studies revealed that NF-κB1 −/− T cells provided SCID mice less protection than wildtype T cells. These results demonstrate an intrinsic role for NF-κB1 in T cell-mediated immunity to Toxoplasma gondii.

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