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RIPK1 and NF- B signaling in dying cells determines cross-priming of CD8+ T cells

Abstract : Dying cells initiate adaptive immunity by providing both antigens and inflammatory stimuli for dendritic cells, which in turn activate CD8(+) T cells through a process called antigen cross-priming. To define how different forms of programmed cell death influence immunity, we established models of necroptosis and apoptosis, in which dying cells are generated by receptor-interacting protein kinase-3 and caspase-8 dimerization, respectively. We found that the release of inflammatory mediators, such as damage-associated molecular patterns, by dying cells was not sufficient for CD8(+) T cell cross-priming. Instead, robust cross-priming required receptor-interacting protein kinase-1 (RIPK1) signaling and nuclear factor κB (NF-κB)-induced transcription within dying cells. Decoupling NF-κB signaling from necroptosis or inflammatory apoptosis reduced priming efficiency and tumor immunity. Our results reveal that coordinated inflammatory and cell death signaling pathways within dying cells orchestrate adaptive immunity.
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Contributor : Marie-Christine Vougny Connect in order to contact the contributor
Submitted on : Thursday, October 13, 2016 - 1:56:45 PM
Last modification on : Monday, May 9, 2022 - 11:58:08 AM

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N. Yatim, H. Jusforgues-Saklani, S. Orozco, O. Schulz, R. Barreira da Silva, et al.. RIPK1 and NF- B signaling in dying cells determines cross-priming of CD8+ T cells. Science, American Association for the Advancement of Science (AAAS), 2015, 350 (6258), pp.328-334. ⟨10.1126/science.aad0395⟩. ⟨pasteur-01380732⟩



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