Supporting data for: <b>Caspase-8 expression in CD8</b>^{<strong>+ </strong>}<b>T cells promotes pathogen restriction in the brain during </b><b><i>Toxoplasma gondii</i></b><b> </b><b>infection </b>(Casp8floxedRipk3 Cre lines)

<p dir="ltr">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, <i>Toxoplasma gondii.</i> Here we focus on the role of caspase-8, a regulator of extrinsic apoptosis, during <i>T. gondii </i>infection. We find that <i>Casp8</i>^<em>-/-</em><i>Ripk3</i>^<em>-/-</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 <i>Casp8</i>^<em>-/-</em><i>Ripk3</i>^<em>-/-</em> mice compared to WT mice. While <i>Casp8 </i>deficiency in neurons and astrocytes did not impact control of infection, deletion of <i>Casp8</i> 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 <i>T. gondii</i> in the brain.</p><p><br></p><p dir="ltr">This item contains raw data that pertains to Casp8FLOXEDRipk3-/- mice with various Cre lines. Data ranges from naive to various time points post T. gondii infection and include flow cytometry based cell population quantifications, RT-PCR quantifications, and parasite burden quantifications. Information regarding date collected, timepoint, sex, and data type can be found in the file title.</p>