Journal
NATURE IMMUNOLOGY
Volume 15, Issue 1, Pages 98-108Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2768
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Funding
- US National Institutes of Health [R01 AI093981, R01 DK084647, R37 AI047822, 5T32AI007290-25, K01 AR59378, AI07290]
- US Department of Veterans Affairs
- Digestive Disease Center of Stanford University [P30 DK056339]
- German Research Foundation
- Crohn's and Colitis Foundation of America
- Stanford Institute for Immunity, Transplantation and Infection
- Agency for Science, Technology And Research of Singapore
- Swiss National Science Foundation [PBBEP3-133516]
- Swiss Foundation for Grants in Biology and Medicine [PASMP3-142725]
- Leukemia & Lymphoma Society
- California Institute for Regenerative Medicine
- Arthritis Foundation
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI047822, R01AI093981, T32AI007290] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [K01AR059378] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK056339, R01DK084647] Funding Source: NIH RePORTER
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Dendritic cells (DCs) that orchestrate mucosal immunity have been studied in mice. Here we characterized human gut DC populations and defined their relationship to previously studied human and mouse DCs. CD103(+)Sirp alpha(-) DCs were related to human blood CD141(+) DCs and to mouse intestinal CD103(+)CD11b(-) DCs and expressed markers of cross-presenting DCs. CD103(+)Sirp alpha(+) DCs aligned with human blood CD1c(+) DCs and mouse intestinal CD103(+)CD11b(+) DCs and supported the induction of regulatory T cells. Both CD103(+) DC subsets induced the T(H)17 subset of helper T cells, while CD103-Sirp alpha(+) DCs induced the T(H)17 subset of helper T cells. Comparative analysis of transcriptomes revealed conserved transcriptional programs among CD103(+) DC subsets and identified a selective role for the transcriptional repressors BcI-6 and Blimp-1 in the specification of CD103(+)CD11b(-) DCs and intestinal CD103(+)CD11b(+) DCs, respectively. Our results highlight evolutionarily conserved and divergent programming of intestinal DCs.
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