Supporting data for:<b> </b><b>Caspase-8 expression in CD8</b><sup><strong>+ </strong></sup><b>T cells promotes pathogen restriction in the brain during</b><b><i> </i></b><b><i>Toxoplasma gondii</i></b><b> </b><b>infection</b> (Casp8Ripk3 KO Images)
<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><sup><em>-/-</em></sup><i>Ripk3</i><sup><em>-/-</em></sup> 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<sup>+</sup> T cells had high rates of parasite interactions in <i>Casp8</i><sup><em>-/-</em></sup><i>Ripk3</i><sup><em>-/-</em></sup> 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<sup>+</sup> T cells led to impaired survival, increased parasite burden and direct infection of CD8<sup>+</sup> T cells in the brain. We conclude that in addition to well-characterized effector functions, CD8<sup>+</sup> T cells utilize caspase-8 to control <i>T. gondii</i> in the brain.</p><p><br></p><p dir="ltr">This item contains immunohistochemistry images that pertain to the Casp8-/-Ripk3-/- experiments. The images are of brain sagittal sections. Information regarding genotype, antibody, and magnification can all be found in the title of the file.</p>
Funding
Alarmin-mediated control of CNS infection
National Institute of Neurological Disorders and Stroke