Evidence map›Paper›PMID 41482545›Full record

ArticleNature immunology2026

Cross-presentation of dead cell-associated antigens shapes the neoantigenic landscape of tumor immunity.

Kok Haw Jonathan Lim, Oliver Schulz, Irene Lobon, Tomas Castro-Dopico, Luis Zapata, Evangelos Giampazolias, Bruno Frederico, Carlos A Castellanos, Michael D Buck, William Stainier and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

21 authors.

Kok Haw Jonathan Lim *Immunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-6544-9218
Oliver Schulz *Immunobiology Laboratory, The Francis Crick Institute, London, UK.
Irene LobonCancer Dynamics Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-1170-9915
Tomas Castro-DopicoImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-6964-5478
Luis ZapataCentre for Evolution and Cancer, Institute of Cancer Research, London, UK.
Evangelos GiampazoliasImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Bruno FredericoImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Carlos A CastellanosImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-3615-2009
Michael D BuckImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-9611-1199
William StainierImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0009-0003-6182-4003
Probir ChakravartyBioinformatics and Biostatistics, The Francis Crick Institute, London, UK.
Gavin KellyBioinformatics and Biostatistics, The Francis Crick Institute, London, UK.ORCID 0000-0001-7219-560X
Neil C RogersImmunobiology Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0001-8977-7585
Ana CardosoImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Sonia LeeImmunobiology Laboratory, The Francis Crick Institute, London, UK.
Brian VashApple Tree Partners, Cambridge, USA.
Stephanie MaioccoApple Tree Partners, Cambridge, USA.
Raj MehtaAdendra Therapeutics Ltd., London, UK.
Jessica StridDepartment of Immunology and Inflammation, Imperial College London, London, UK.
Samra TurajlićCancer Dynamics Laboratory, The Francis Crick Institute, London, UK.
Caetano Reis E SousaImmunobiology Laboratory, The Francis Crick Institute, London, UK. caetano@crick.ac.uk.ORCID 0000-0001-7392-2119

Funding

Deciphering Clonal Evolution in Hereditary Renal Cell CarcinomasU01CA247439 · NCI · FRANCIS CRICK INSTITUTE, LTD · PI TURAJLIC, SAMRA · 2020 to 2024
$1.1M
EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) AdG 268670NCI NIH HHS U01 CA247439Wellcome Trust CC2090Wellcome Trust (Wellcome) 106973/Z/15/ZWellcome Trust (Wellcome) 216327/Z/19/Z
6 · The paper itself

Abstract

Type 1 conventional dendritic cells (cDC1s) acquire and cross-present tumor antigens to prime CD8⁺ T cells. Whether this selects for specific neoantigens is unclear. DNGR-1 (CLEC9A), a cDC1 receptor for F-actin exposed on dead cells, promotes cross-presentation of cell-associated antigens. Here we show that DNGR-1-deficient mice develop chemically induced tumors more rapidly and at higher incidence, and these are more frequently rejected on transplantation into wild-type recipients. Whole-exome sequencing reveals enrichment of predicted neoantigens derived from mutated F-actin-binding proteins. Consistent with this observation, tethering model antigens to F-actin enhances DNGR-1-dependent cross-presentation. These results suggest that DNGR-1-mediated recognition of F-actin exposed by dead cancer cells favors priming of CD8⁺ T cells specific for cytoskeletal neoantigens, which can then drive immune escape of cancer cells lacking or reverting those mutations. Thus, neoantigen cross-presentation by cDC1 can determine the immune visibility of the tumor mutational landscape and sculpt cancer evolution by immunoediting.

Indexed as

Antigens, NeoplasmCD8-Positive T-LymphocytesCross-PrimingDendritic CellsLectins, C-TypeNeoplasmsActinsAnimalsHumansMiceMice, Inbred C57BLMice, KnockoutMutationReceptors, ImmunologicTumor EscapeActinsAntigens, NeoplasmClec9a protein, mouseLectins, C-TypeReceptors, Immunologic

Identifiers

PMID41482545
PMCPMC12764433

What OpenQuestion holds

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Registered trials

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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.