| First Author | Calzada-Fraile D | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 6772 |
| PubMed ID | 37880206 | Mgi Jnum | J:342049 |
| Mgi Id | MGI:7544527 | Doi | 10.1038/s41467-023-42480-3 |
| Citation | Calzada-Fraile D, et al. (2023) Immune synapse formation promotes lipid peroxidation and MHC-I upregulation in licensed dendritic cells for efficient priming of CD8(+) T cells. Nat Commun 14(1):6772 |
| abstractText | Antigen cognate dendritic cell (DC)-T cell synaptic interactions drive activation of T cells and instruct DCs. Upon receiving CD4(+) T cell help, post-synaptic DCs (psDCs) are licensed to generate CD8(+) T cell responses. However, the cellular and molecular mechanisms that enable psDCs licensing remain unclear. Here, we describe that antigen presentation induces an upregulation of MHC-I protein molecules and increased lipid peroxidation on psDCs in vitro and in vivo. We also show that these events mediate DC licensing. In addition, psDC adoptive transfer enhances pathogen-specific CD8(+) T responses and protects mice from infection in a CD8(+) T cell-dependent manner. Conversely, depletion of psDCs in vivo abrogates antigen-specific CD8(+) T cell responses during immunization. Together, our data show that psDCs enable CD8(+) T cell responses in vivo during vaccination and reveal crucial molecular events underlying psDC licensing. |
