Journal
IMMUNITY
Volume 53, Issue 2, Pages 335-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2020.06.002
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Funding
- National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London
- BBSRC
- CRUK
- Rosetrees Trust
- CRUK King's Health Partners Cancer Centre in United Kingdom
- IDEX [ANR-18-IDEX-0001]
- INCA (PL-BIO-ICR1)
- Institut Curie, Institut National de la Sante' et de la Recherche Medicale [ANR-10-IDEX-0001-02 PSL, ANR-11LABX0043]
- Programa de Apoyo a Centros con Financiamiento Basal [AFB 170004]
- FONDECYT in Chile [1171703]
- NC3RS
- Labex DCBIOL
- BBSRC [BB/M029735/1] Funding Source: UKRI
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Dendritic cells (DCs) are antigen-presenting cells controlling T cell activation. In humans, the diversity, ontogeny, and functional capabilities of DC subsets are not fully understood. Here, we identified circulating CD88(-)CD1c(+)CD163(+) DCs (called DC3s) as immediate precursors of inflammatory CD88(-)CD14(+)CD1c(+) CD163(+)Fc epsilon RI+ DCs. DC3s develop via a specific pathway activated by GM-CSF, independent of cDC-restricted (CDP) and monocyte-restricted (cMoP) progenitors. Like classical DCs but unlike monocytes, DC3s drove activation of naive T cells. In vitro, DC3s displayed a distinctive ability to prime CD8(+) T cells expressing a tissue homing signature and the epithelial homing alpha-E integrin (CD103) through transforming growth factor beta (TGF-beta) signaling. In vivo, DC3s infiltrated luminal breast cancer primary tumors, and DC3 infiltration correlated positively with CD8(+)CD103(+)CD69(+) tissue-resident memory T cells. Together, these findings define DC3s as a lineage of inflammatory DCs endowed with a strong potential to regulate tumor immunity.
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