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Human dendritic cell subsets: an update
Open accessAbstract
Dendritic cells (DC) are a class of bone-marrow-derived cells arising from lympho-myeloid haematopoiesis that form an essential interface between the innate sensing of pathogens and the activation of adaptive immunity. This task requires a wide range of mechanisms and responses, which are divided between three major DC subsets: plasmacytoid DC (pDC), myeloid/conventional DC1 (cDC1) and myeloid/conventional DC2 (cDC2). Each DC subset develops under the control of a specific repertoire of transcription factors involving differential levels of IRF8 and IRF4 in collaboration with PU.1, ID2, E2-2, ZEB2, KLF4, IKZF1 and BATF3. DC haematopoiesis is conserved between mammalian species and is distinct from monocyte development. Although monocytes can differentiate into DC, especially during inflammation, most quiescent tissues contain significant resident populations of DC lineage cells. An extended range of surface markers facilitates the identification of specific DC subsets although it remains difficult to dissociate cDC2 from monocyte-derived DC in some settings. Recent studies based on an increasing level of resolution of phenotype and gene expression have identified pre-DC in human blood and heterogeneity among cDC2. These advances facilitate the integration of mouse and human immunology, support efforts to unravel human DC function in vivo and continue to present new translational opportunities to medicine.
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“The three other proteins increased in abundance in TET2-CH were CD1C (a marker of conventional dendritic cells), CLEC4C (a marker of plasmacytoid dendritic cells) and CD86 (a marker of dendritic cells, monocytes and other antigen-presenting cells)51.”
From Rare variant associations with plasma protein levels in the UK Biobank (2023) · cites this paper as [51]
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“pDCs are instead characterized by a marked impairment of cytokine release in older people (27, 29).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [27]
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Metadata
- Authors
- Collin, M., & Bigley, V.
- Affiliations
- Newcastle upon Tyne Hospitals NHS Foundation Trust (GB)
- Corresponding author
- Collin, Matthew
- Venue
- Immunology
- Publisher
- Wiley
- Published
- 2018-02-27
- Volume
- 154
- Issue
- 1
- Pages
- 3-20
- ISSN
- 0019-2805 (ISSN-L)
- 1365-2567
- PMC
- PMC5904714
- OpenAlex
- W2781617771
- Cited by
- 1,301
- References
- 203
- Citations by year
- 2026: 69 · 2025: 169 · 2024: 167 · 2023: 191 · 2022: 237 · 2021: 198 · 2020: 155 · 2019: 87 · 2018: 27
- FWCI
- 11.83
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- Cancer Research UK (C30484/A21025)
- Wellcome Trust (101155/Z/13/Z)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- dendritic cells, dendritic cell subsets, plasmacytoid dendritic cells, myeloid dendritic cells, DC1, DC2, transcription factors, IRF8, IRF4, PU.1, monocyte-derived dendritic cells, cell surface markers, innate immunity, adaptive immunity
- MeSH terms
- Kruppel-Like Factor 4, Cell Communication, Cell Differentiation, Dendritic Cells, Humans, Immunity, Phenotype, Signal Transduction, Biomarkers, Immunophenotyping
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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