Supporting data for: Caspase-8 expression in CD8+ T cells promotes pathogen restriction in the brain during Toxoplasma gondii infection

<p>  </p> <p>Cell death is an integral restriction mechanism against intracellular pathogens. We have previously reported extensive cell death in the brain during infection with the intracellular parasite, <em>Toxoplasma gondii.</em> Here we focus on the role of caspase-8, a regulator of extrinsic apoptosis, during <em>T. gondii </em>infection. We find that <em>Casp8-/-Ripk3-/-</em> mice have increased brain parasite burden in comparison to controls and succumb to infection, despite the generation of robust immune responses. We observed that neurons, astrocytes, and CD8+ T cells had high rates of parasite interactions in <em>Casp8-/-Ripk3-/-</em> mice compared to WT mice. While <em>Casp8 </em>deficiency in neurons and astrocytes did not impact control of infection, deletion of <em>Casp8</em> in CD8+ T cells led to impaired survival, increased parasite burden and direct infection of CD8+ T cells in the brain. We conclude that in addition to well-characterized effector functions, CD8+ T cells utilize caspase-8 to control <em>T. gondii</em> in the brain.</p>