Evidence map›Paper›PMID 40968162›Full record

ArticleNature immunology2025

Epigenetic imprinting in innate lymphoid cell precursors directs the lineage segregation of innate lymphoid cells.

Zhen Liu, Fei Shao, Qiang Zhang, Min Zhao, Shuai Gao, Xusheng Zhang, Dou Yu, Jingyao Zhang, Pengyan Xia, Shuo Wang

Abstract read
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In one paragraph

Article in Nature immunology, 2025. 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

10 authors.

Zhen Liu *Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Fei Shao *Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Qiang Zhang *Institute of Cardiovascular Diseases, Xiamen Cardiovascular Hospital, School of Medicine, Xiamen University, Xiamen, China.
Min ZhaoLaboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Shuai GaoState Key Laboratory of Animal Biotech Breeding, Frontiers Science Center for Molecular Design Breeding (MOE), College of Animal Science and Technology, China Agricultural University, Beijing, China.
Xusheng ZhangLaboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Dou YuLaboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Jingyao ZhangState Key Laboratory of Animal Biotech Breeding, Frontiers Science Center for Molecular Design Breeding (MOE), College of Animal Science and Technology, China Agricultural University, Beijing, China.
Pengyan XiaDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.ORCID http://orcid.org/0000-0001-7959-5796
Shuo WangLaboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China. wangshuo@im.ac.cn.ORCID http://orcid.org/0000-0002-5383-3386

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) are essential for mucosal homeostasis, but the epigenetic regulation of their lineage segregation remains elusive. Here we simultaneously profiled the single-cell DNA methylome, chromatin accessibility and transcriptome of ILC subsets and ILC precursors (ILCPs) and found that ILCPs could be divided into two subgroups (ILCP1 and ILCP2). ILCP2s had highly heterogeneous DNA methylation profiles and could be divided into three groups according to their DNA methylation characteristics, which matched those of ILC subsets. We identified the signature methylation regions (SMRs) of each ILC subset and traced the DNA methylation imprinting during ILCP differentiation. ILCP2s with hypomethylated SMRs characteristic of ILC subsets differentiated into those subsets. DNA methylation editing of SMRs suppressed ILC lineage segregation, while deletion of Dnmt1 in ILCPs abrogated the heterogeneous distribution of SMRs and resulted in ILC differentiation defects. These findings provide evidence that epigenetic imprinting determines lineage segregation during immune cell development.

Indexed as

Cell LineageEpigenesis, GeneticGenomic ImprintingImmunity, InnateLymphocytesLymphoid Progenitor CellsAnimalsCell DifferentiationDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationMiceMice, Inbred C57BLMice, KnockoutSingle-Cell AnalysisDNA (Cytosine-5-)-Methyltransferase 1

Identifiers

PMID40968162

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.