Evidence map›Paper›PMID 37308670›Full record

ArticleNature genetics2023

Mapping interindividual dynamics of innate immune response at single-cell resolution.

Natsuhiko Kumasaka, Raghd Rostom, Ni Huang, Krzysztof Polanski, Kerstin B Meyer, Sharad Patel, Rachel Boyd, Celine Gomez, Sam N Barnett, Nikolaos I Panousis and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Nature genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
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

27 citing papers in PubMed, 43 citations in OpenAlex.

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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

26 authors at 9 institutions in 4 countries.

Natsuhiko KumasakaWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-3557-0375
Raghd RostomWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Ni HuangWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Krzysztof PolanskiWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-2586-9576
Kerstin B MeyerWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0001-5906-1498
Sharad PatelWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Rachel BoydWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Celine GomezWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Sam N BarnettWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-8968-4319
Nikolaos I PanousisWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Jeremy SchwartzentruberWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Maya GhoussainiWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-2415-2143
Paul A LyonsCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0001-7035-8997
Fernando J Calero-NietoWellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-3358-8253
Berthold GöttgensWellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0001-6302-5705
Josephine L BarnesUCL Respiratory, Division of Medicine, University College London, London, UK.ORCID http://orcid.org/0000-0001-9938-3176
Kaylee B WorlockUCL Respiratory, Division of Medicine, University College London, London, UK.ORCID http://orcid.org/0000-0002-5656-7634
Masahiro YoshidaUCL Respiratory, Division of Medicine, University College London, London, UK.ORCID http://orcid.org/0000-0002-3521-5322
Marko Z NikolićUCL Respiratory, Division of Medicine, University College London, London, UK.ORCID http://orcid.org/0000-0001-6304-6848
Emily StephensonWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
Gary ReynoldsBiosciences Institute, Newcastle University, Newcastle upon Tyne, UK.ORCID http://orcid.org/0000-0002-8142-8708
Muzlifah HaniffaWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-3927-2084
John C MarioniWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0001-9092-0852
Oliver StegleWellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK.ORCID http://orcid.org/0000-0002-8818-7193
Tzachi Hagai *Shmunis School of Biomedicine and Cancer Research, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel. tzachiha@tauex.tau.ac.il.ORCID http://orcid.org/0000-0002-4575-6624
Sarah A Teichmann *Wellcome Sanger Institute, Wellcome Genome Campus, Cambridge, UK. st9@sanger.ac.uk.ORCID http://orcid.org/0000-0002-6294-6366
Wellcome Sanger Institute · GBEuropean Bioinformatics Institute · GBUniversity College London · GBUniversity of Cambridge · GBWellcome/MRC Cambridge Stem Cell Institute · GBNewcastle University · GBNewcastle upon Tyne Hospitals NHS Foundation Trust · GBTel Aviv University · ILUniversity College London Hospitals NHS Foundation Trust · GB

Funding

Department of HealthMedical Research Council MC_PC_17230Medical Research Council MR/5005579/1Medical Research Council MR/R015635/1Medical Research Council MR/S036113/1Medical Research Council MR/W00111X/1Wellcome Trust 206328/Z/17/ZWellcome Trust WT206194
6 · The paper itself

Abstract

Common genetic variants across individuals modulate the cellular response to pathogens and are implicated in diverse immune pathologies, yet how they dynamically alter the response upon infection is not well understood. Here, we triggered antiviral responses in human fibroblasts from 68 healthy donors, and profiled tens of thousands of cells using single-cell RNA-sequencing. We developed GASPACHO (GAuSsian Processes for Association mapping leveraging Cell HeterOgeneity), a statistical approach designed to identify nonlinear dynamic genetic effects across transcriptional trajectories of cells. This approach identified 1,275 expression quantitative trait loci (local false discovery rate 10%) that manifested during the responses, many of which were colocalized with susceptibility loci identified by genome-wide association studies of infectious and autoimmune diseases, including the OAS1 splicing quantitative trait locus in a COVID-19 susceptibility locus. In summary, our analytical approach provides a unique framework for delineation of the genetic variants that shape a wide spectrum of transcriptional responses at single-cell resolution.

Indexed as

Autoimmune DiseasesCOVID-19Genome-Wide Association StudyHumansImmunity, Innate

Identifiers

PMID37308670
PMCPMC10260404
OpenAlexW4380369163

What OpenQuestion holds

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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.