Evidence map›Paper›PMID 39923740›Full record

ArticleEBioMedicine2025

Neolithic introgression of IL23R-related protection against chronic inflammatory bowel diseases in modern Europeans.

Ben Krause-Kyora, Nicolas Antonio da Silva, Elif Kaplan, Daniel Kolbe, Archaeological Civilization Disease Consortium (ACDC), Inken Wohlers, Hauke Busch, David Ellinghaus, Amke Caliebe, Efe Sezgin and 2 more

Abstract read
In one paragraph

Article in EBioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
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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

12 authors.

Ben Krause-KyoraInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany. Electronic address: b.krause-kyora@ikmb.uni-kiel.de.
Nicolas Antonio da SilvaInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Elif KaplanInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Daniel KolbeInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Archaeological Civilization Disease Consortium (ACDC)
Inken WohlersBiomolecular Data Science in Pneumology, Research Center Borstel, Borstel, Germany; University of Lübeck, Lübeck, Germany.
Hauke BuschLübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
David EllinghausInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Amke CaliebeInstitute of Medical Informatics and Statistics, Kiel University, Kiel, Germany.
Efe SezginDepartment of Food Engineering, Izmir Institute of Technology, Urla, Izmir, Turkey.
Almut NebelInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany.
Stefan SchreiberInstitute of Clinical Molecular Biology, Kiel University, Kiel, Germany; Department for Medicine I, Kiel University, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. Electronic address: s.schreiber@mucosa.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe hypomorphic variant rs11209026-A in the IL23R gene provides significant protection against immune-related diseases in Europeans, notably inflammatory bowel diseases (IBD). Today, the A-allele occurs with an average frequency of 5% in Europe.

methodsThis study comprised 251 ancient genomes from Europe spanning over 14,000 years. In these samples, the investigation focused on admixture-informed analyses and selection scans of rs11209026-A and its haplotypes.

findingsrs11209026-A was found at high frequencies in Anatolian Farmers (AF, 18%). AF later introduced the allele into the ancient European gene-pool. Subsequent admixture caused its frequency to decrease and formed the current southwest-to-northeast allele frequency cline in Europe. The geographic distribution of rs11209026-A may influence the gradient in IBD incidence rates that are highest in northern and eastern Europe.

interpretationGiven the dramatic changes from hunting and gathering to agriculture during the Neolithic, AF might have been exposed to selective pressures from a pro-inflammatory lifestyle and diet. Therefore, the protective A-allele may have increased survival by reducing intestinal inflammation and microbiome dysbiosis. The adaptively evolved function of the variant likely contributes to the high efficacy and low side-effects of modern IL-23 neutralisation therapies for chronic inflammatory diseases.

fundingGerman Research Foundation (EXC 2167 390884018 and EXC 2150 390870439).

Indexed as

Genetic Predisposition to DiseaseInflammatory Bowel DiseasesReceptors, InterleukinWhite PeopleAllelesEuropeEuropean PeopleGene FrequencyHaplotypesHumansPolymorphism, Single NucleotideIL23R protein, humanReceptors, InterleukinAncient genomicsCrohn's diseaseIL23RIL-23-signallingInflammatory bowel diseasesUlcerative colitis

Identifiers

PMID39923740
PMCPMC11849592

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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.