期刊
SCIENCE
卷 350, 期 6258, 页码 328-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad0395
关键词
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资金
- Agence Nationale de Recherches sur le Sida et les Hepatitis
- Agence Nationale de la Recherche [ANR-12-BSV3-0011-01]
- Laboratories of Excellence Immuno-Onco grant [ANR-11-IDEX-0005-02]
- French National Cancer Institute (INCa)
- Ecole de l'Inserm Liliane Bettencourt
- NIH [R21CA185681, R01AI108685, AI44848, 5R01AI108685-02]
- Cancer Research UK
- Francis Crick Institute
- European Research Council
- Genomics Platform of the Department of Translational Research at Institut Curie [INCa-DGOS-4654, SIRIC11-002, ANR-10-IDEX-0001-02 PSL, ANR-11-LBX-0044]
- Agence Nationale de la Recherche (ANR) [ANR-12-BSV3-0011] Funding Source: Agence Nationale de la Recherche (ANR)
- Cancer Research UK [15689] Funding Source: researchfish
- The Francis Crick Institute [10136] Funding Source: researchfish
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 kappa B (NF-kappa B)-induced transcription within dying cells. Decoupling NF-kappa B 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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