| First Author | Yatim N | Year | 2015 |
| Journal | Science | Volume | 350 |
| Issue | 6258 | Pages | 328-34 |
| PubMed ID | 26405229 | Mgi Jnum | J:318341 |
| Mgi Id | MGI:6859279 | Doi | 10.1126/science.aad0395 |
| Citation | Yatim N, et al. (2015) RIPK1 and NF-kappaB signaling in dying cells determines cross-priming of CD8(+) T cells. Science 350(6258):328-34 |
| abstractText | 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 kappaB (NF-kappaB)-induced transcription within dying cells. Decoupling NF-kappaB 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. |
