Journal
IMMUNITY
Volume 45, Issue 4, Pages 847-860Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.08.019
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Funding
- NIH Tetramer Core Facility [HHSN272201300006C]
- CNIC
- Spanish Ministry of Economy and Competitiveness (MINECO) [SAF-2013-42920R]
- European Commission [635122-PROCROP H2020]
- European Research Council [ERC-2010-StG 260414]
- MINECO
- Pro-CNIC Foundation
- Severo Ochoa Center of Excellence (MINECO award) [SEV-2015-0505]
- [SAF2015-74561-JIN]
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Despite the crucial role of tissue-resident memory T (Trm) cells in protective immunity, their priming remains poorly understood. Here, we have shown differential priming requirements for Trm versus circulating memory CD8(+) T cells. In vaccinia cutaneous- infected mice, DNGR-1-mediated crosspresentation was required for optimal Trm cell priming but not for their skin differentiation or for circulating memory T cell generation. DNGR-1(+) dendritic cells (DCs) promoted T-bet transcription-factor induction and retention of CD8(+) T cells in the lymph nodes (LNs). Inhibition of LN egress enhanced Trm cell generation, whereas genetic or antibody blockade of DNGR-1 or specific signals provided during priming by DNGR-1(+) DCs, such as interleukin-12 (IL-12), IL-15, or CD24, impaired Trm cell priming. DNGR-1 also regulated Trm cell generation during influenza infection. Moreover, protective immunity depended on optimal Trm cell induction by DNGR-1(+) DCs. Our results reveal specific priming requirements for CD8(+) Trm cells during viral infection and vaccination.
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