The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Identification of a dendritic cell receptor that couples sensing of necrosis to immunity
Open accessAbstract
Injury or impaired clearance of apoptotic cells leads to the pathological accumulation of necrotic corpses, which induce an inflammatory response that initiates tissue repair. In addition, antigens present in necrotic cells can sometimes provoke a specific immune response and it has been argued that necrosis could explain adaptive immunity in seemingly infection-free situations, such as after allograft transplantation or in spontaneous and therapy-induced tumour rejection. In the mouse, the CD8alpha+ subset of dendritic cells phagocytoses dead cell remnants and cross-primes CD8+ T cells against cell-associated antigens. Here we show that CD8alpha+ dendritic cells use CLEC9A (also known as DNGR-1), a recently-characterized C-type lectin, to recognize a preformed signal that is exposed on necrotic cells. Loss or blockade of CLEC9A does not impair the uptake of necrotic cell material by CD8+ dendritic cells, but specifically reduces cross-presentation of dead-cell-associated antigens in vitro and decreases the immunogenicity of necrotic cells in vivo. The function of CLEC9A requires a key tyrosine residue in its intracellular tail that allows the recruitment and activation of the tyrosine kinase SYK, which is also essential for cross-presentation of dead-cell-associated antigens. Thus, CLEC9A functions as a SYK-coupled C-type lectin receptor to mediate sensing of necrosis by the principal dendritic-cell subset involved in regulating cross-priming to cell-associated antigens.
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In the citing paper
“The activation of caspases, a specific class of cysteine proteases has multiple effects on the immunogenicity of cell death 56”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“Necrosis has traditionally been considered merely as an accidental, uncontrolled form of cell death that only occurs in pathological circumstances.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“There are several distinct subtypes of apoptosis that, although morphologically similar, can be triggered through different biochemical routes (for example, through the intrinsic or the extrinsic pathway or with or without caspase activation).”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“Necrosis is morphologically characterized by a gain in cell volume (oncosis), swelling of organelles, plasma membrane rupture and subsequent loss of intracellular contents.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“Autophagic cell death occurs in the absence of chromatin condensation but is accompanied by massive autophagic vacuolization of the cytoplasm.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“Apoptosis is accompanied by rounding-up of the cell, retraction of pseudopods, reduction of cellular volume (pyknosis), chromatin condensation, nuclear fragmentation (karyorrhexis), few or no ultrastructural modifications of cytoplasmic organelles, and plasma membrane blebbing but cell integrity is maintained until the final stages of the process.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“Furthermore, the apparent uniformity of apoptotic cell death may conceal heterogeneous functional aspects, such as whether or not dying apoptotic cells are recognized by the immune system 56.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [56]
In the citing paper
“CLeC9A has been shown to recognize necrotic cells and induce the cross-presentation of dead cell-associated antigens to CD8+ T cells.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [75]
In the citing paper
“Therefore, it may be involved in regulating sterile immune responses, although the specific ligand recognized in this case is still unknown73,75.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [75]
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Metadata
- Authors
- Sancho, D., Joffre, O. P., Keller, A. M., Rogers, N. C., Martínez, D., Hernanz-Falcón, P., Rosewell, I., & Sousa, C. R. E.
- Affiliations
- The Honourable Society of Lincoln's Inn (GB)
- Cancer Research UK (GB)
- Corresponding author
- Sousa, Caetano Reis e
- Venue
- Nature
- Published
- 2009-04
- Volume
- 458
- Issue
- 7240
- Pages
- 899-903
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2671489
- OpenAlex
- W2136883776
- Cited by
- 750
- References
- 27
- Citations by year
- 2026: 17 · 2025: 35 · 2024: 31 · 2023: 44 · 2022: 45 · 2021: 39 · 2020: 44 · 2019: 38 · 2018: 37 · 2017: 30 · 2016: 47 · 2015: 49 · 2014: 54 · 2013: 55 · 2012: 61
- FWCI
- 26.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Cancer Research UK (A3598)
- 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 › Phagocytosis and Immune Regulation
- Keywords
- CLEC9A, DNGR-1, C-type lectin receptors, dendritic cells, CD8α+ dendritic cells, necrosis, cross-presentation, Syk, immunogenicity, tissue repair, inflammation, allograft rejection, tumor rejection
- MeSH terms
- Animals, Cells, Cultured, Dendritic Cells, Humans, Ligands, Necrosis, Phagocytosis, Receptors, Immunologic, Receptors, Mitogen, Signal Transduction, CD8 Antigens, CD8-Positive T-Lymphocytes, Lectins, C-Type, Cross-Priming, Mice
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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