Evidence map›Paper›PMID 34437840›Full record

ArticleImmunity2021

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection.

Sophie Flommersfeld, Jan P Böttcher, Jonatan Ersching, Michael Flossdorf, Philippa Meiser, Ludwig O Pachmayr, Justin Leube, Inge Hensel, Sebastian Jarosch, Qin Zhang and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 78 citations in OpenAlex.

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  5. LAG3 Marks Activated but Hyporesponsive NK Cells.European journal of immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 9 institutions in 2 countries.

Sophie FlommersfeldInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Jan P BöttcherInstitute of Molecular Immunology and Experimental Oncology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich (TUM), Munich, Germany.
Jonatan ErschingLaboratory of Lymphocyte Dynamics, The Rockefeller University, New York, NY 10065, USA.
Michael FlossdorfInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Philippa MeiserInstitute of Molecular Immunology and Experimental Oncology, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich (TUM), Munich, Germany.
Ludwig O PachmayrInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Justin LeubeInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Inge HenselInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Sebastian JaroschInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Qin ZhangDivision of Theoretical Systems Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany; BioQuant Center, University of Heidelberg, Heidelberg, Germany.
M Zeeshan ChaudhryHelmholtz Centre for Infection Research, Braunschweig, Germany.
Immanuel AndraeInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Matthias SchiemannInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany.
Dirk H BuschInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany; German Center for Infection Research (DZIF), Partner Site Munich, Munich, Germany.
Luka Cicin-SainHelmholtz Centre for Infection Research, Braunschweig, Germany.
Joseph C SunImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Georg GasteigerWürzburg Institute of Systems Immunology, Würzburg, Germany; Max Planck Research Group at the Julius-Maximilians-Universität Würzburg, Würzburg, Germany.
Gabriel D VictoraLaboratory of Lymphocyte Dynamics, The Rockefeller University, New York, NY 10065, USA.
Thomas HöferDivision of Theoretical Systems Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany; BioQuant Center, University of Heidelberg, Heidelberg, Germany.
Veit R BuchholzInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany; German Center for Infection Research (DZIF), Partner Site Munich, Munich, Germany. Electronic address: veit.buchholz@tum.de.
Simon GrassmannInstitute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich (TUM), Munich, Germany; Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: simon.grassmann@tum.de.
Technical University of Munich · DEInstitute of Medical Microbiology and Hygiene · DEHeidelberg University · DEHelmholtz Centre for Infection Research · DERockefeller University · USGerman Center for Infection Research · DEKlinikum rechts der Isar · DEMemorial Sloan Kettering Cancer Center · USUniversity of Würzburg · DE

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
European Research Council 949719NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Upon viral infection, natural killer (NK) cells expressing certain germline-encoded receptors are selected, expanded, and maintained in an adaptive-like manner. Currently, these are thought to differentiate along a common pathway. However, by fate mapping of single NK cells upon murine cytomegalovirus (MCMV) infection, we identified two distinct NK cell lineages that contributed to adaptive-like responses. One was equivalent to conventional NK (cNK) cells while the other was transcriptionally similar to type 1 innate lymphoid cells (ILC1s). ILC1-like NK cells showed splenic residency and strong cytokine production but also recognized and killed MCMV-infected cells, guided by activating receptor Ly49H. Moreover, they induced clustering of conventional type 1 dendritic cells and facilitated antigen-specific T cell priming early during MCMV infection, which depended on Ly49H and the NK cell-intrinsic expression of transcription factor Batf3. Thereby, ILC1-like NK cells bridge innate and adaptive viral recognition and unite critical features of cNK cells and ILC1s.

Indexed as

Adaptive ImmunityAnimalsCell LineageFemaleHerpesviridae InfectionsImmunity, InnateKiller Cells, NaturalMaleMiceMice, Inbred BALB CMice, Inbred C57BLMuromegalovirusadaptive-like NK cell responsesILC1ILC1-like NK cellsMCMVNK cellssingle-cell fate mapping

Identifiers

PMID34437840
PMCPMC8528403
OpenAlexW3194594621

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.