Culling of APCs by inflammatory cell death pathways restricts TIM3 and PD-1 expression and promotes the survival of primed CD8 T cells

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  1. Get@NRC: Culling of APCs by inflammatory cell death pathways restricts TIM3 and PD-1 expression and promotes the survival of primed CD8 T cells (Opens in a new window)
DOIResolve DOI: http://doi.org/10.1038/cdd.2017.112
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TypeArticle
Journal titleCell Death and Differentiation
ISSN1350-9047
1476-5403
AbstractWe evaluated the impact of premature cell death of antigen-presenting cells (APCs) by Caspase-1- and RipK3-signaling pathways on CD8+ T-cell priming during infection of mice with Salmonella typhimurium (ST). Our results indicate that Caspase1 and RipK3 synergize to rapidly eliminate infected APCs, which does not influence the initial activation of CD8+ T cells. However, the maintenance of primed CD8+ T cells was greatly compromised when both these pathways were disabled. Caspase-1- and RipK3-signaling did not influence NF-κB signaling in APCs, but synergized to promote processing of IL-1 and IL-18. Combined deficiency of Caspase1 and RipK3 resulted in compromised innate immunity and accelerated host fatality due to poor processing of IL-18. In contrast, synergism in cell death by Caspase-1- and RipK3 resulted in restriction of PD-1 and TIM3 expression on primed CD8+ T cells, which promoted the survival of activated CD8+ T cells.
Publication date
PublisherNature Publishing Group
LanguageEnglish
AffiliationHuman Health Therapeutics; National Research Council Canada
Peer reviewedYes
NPARC number23002198
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Record identifierdb2c93a2-941f-4ca9-b049-dc978e1911fa
Record created2017-09-01
Record modified2017-09-01
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