Evidence map›Paper›PMID 41162754›Full record

ArticleThe EMBO journal2025

DNGR-1 signalling limits dendritic cell activation for optimal antigen cross-presentation.

Michael D Buck, Tomás Castro-Dopico, Oliver Schulz, Ana Cardoso, Probir Chakravarty, Nathalie Legrave, Conor M Henry, Johnathan Canton, Estelle Wu, Sonia Lee and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Michael D BuckImmunobiology Laboratory, The Francis Crick Institute, London, UK. michael.buck@crick.ac.uk.ORCID http://orcid.org/0000-0002-9611-1199
Tomás Castro-DopicoImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-6964-5478
Oliver SchulzImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Ana CardosoImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-4610-4337
Probir ChakravartyBioinformatics and Biostatistics, The Francis Crick Institute, London, UK.
Nathalie LegraveMetabolomics, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0003-1172-4955
Conor M HenryImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Johnathan CantonImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Estelle WuImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-6197-6694
Sonia LeeImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Neil C RogersImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0001-8977-7585
Enzo Z PoirierImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0001-9795-2144
William StainierImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0009-0003-6182-4003
Victor BosteelsImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Eleanor ChildsImmunobiology Laboratory, The Francis Crick Institute, London, UK.
James I MacRaeMetabolomics, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-1464-8583
J Mark SkehelProteomics, The Francis Crick Institute, London, UK.
Santiago ZelenayCancer Inflammation and Immunity Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester, UK.ORCID http://orcid.org/0000-0002-6865-3978
Caetano Reis E SousaImmunobiology Laboratory, The Francis Crick Institute, London, UK. caetano@crick.ac.uk.ORCID http://orcid.org/0000-0001-7392-2119

Funding

EC | ERC | HORIZON EUROPE European Research Council (ERC) AdG 268670EC | Horizon Europe | Excellent Science | HORIZON EUROPE Marie Sklodowska-Curie Actions (MSCA) 792770EC | Horizon Europe | Excellent Science | HORIZON EUROPE Marie Sklodowska-Curie Actions (MSCA) 837951Wellcome Trust CC2090Wellcome Trust FC001136Wellcome Trust (WT) 106973/Z/15/ZWellcome Trust (WT) 223136/Z/21/Z
6 · The paper itself

Abstract

Innate immune receptors often induce activation of conventional dendritic cells (cDCs) and enhance antigen (cross-)presentation, favouring immune responses. DNGR-1 (CLEC9A), a receptor expressed by type 1 cDCs (cDC1s) and implicated in immune responses to viruses and cancer, recognises F-actin exposed on dead cell remnants and promotes cross-presentation of associated antigens. Here, we show that recruitment of phosphatase SHIP1, a process governed by a single amino acid residue adjacent to the signalling motif of the receptor, partly explains how DNGR-1 fails to trigger cDC1 activation in vitro. Substituting this residue converts DNGR-1 into an activating receptor but decreases induction of cross-presentation of dead cell-associated antigens. Introducing the reverse mutation into the related receptor Dectin-1 impairs its activation capacity while enhancing its ability to promote cross-presentation. These findings reveal a functional trade-off in receptor signalling and suggest that DNGR-1 has evolved to prioritise antigen cross-presentation over cellular activation, possibly to minimise inflammatory responses to dead cells.

Indexed as

Antigen PresentationCross-PrimingDendritic CellsLectins, C-TypeReceptors, ImmunologicSignal TransductionAnimalsDectin-1HumansMiceReceptors, MitogenCLEC9a protein, humanClec9a protein, mouseDectin-1Lectins, C-TypeReceptors, ImmunologicReceptors, MitogenActivationcDC1CLEC9ACross-presentationDNGR-1

Identifiers

PMID41162754
PMCPMC12669754

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.