Evidence map›Paper›PMID 40749046›Full record

ArticleScience advances2025

BACH2 drives the development and function of group 2 innate lymphoid cells.

Gaoyu Liu, Ying Wang, Xianfu Yi, Jianye Wang, Jun Zhang, Xixi Feng, Haitao Wang, Chun Chen, Qiang Liu, Jun Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Gaoyu LiuDepartment of Oncology, Laboratory of Immunity, Inflammation & Cancer, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0001-8487-2815
Ying WangDepartment of Oncology, Laboratory of Immunity, Inflammation & Cancer, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xianfu YiDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-8094-2676
Jianye WangTianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jun ZhangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai Key Laboratory of Pancreatic Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.
Xixi FengState Key Laboratory of Respiratory Disease, the GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China.ORCID 0009-0006-3539-6043
Haitao WangDepartment of Oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases, Tianjin 300211, China.
Chun ChenDivision of Hematology/Oncology, Department of Pediatrics, Shenzhen Key Laboratory of Bone Tissue Repair and Translational Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Qiang LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0002-6621-0591
Jun WangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai Key Laboratory of Pancreatic Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.ORCID 0000-0003-4322-1551
Jie ZhouDepartment of Oncology, Laboratory of Immunity, Inflammation & Cancer, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0001-5964-1599

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group 2 innate lymphoid cells (ILC2s) represent one of the major drivers of allergic inflammation; however, the precise mechanisms governing the development and function of ILC2s remain unknown. Here, we show that the transcription factor BACH2 was abundantly expressed and epigenetically activated in ILC2s and their progenitors. Conditional ablation of BACH2 diminished the ability of ILC2 progenitors to differentiate into ILC2s. Integration of the scRNA-seq, ATAC-seq, and CUT&Tag-seq techniques revealed that BACH2 modulated the transcriptional profiles and epigenetic landscapes of ILC2 progenitors. Furthermore, BACH2 ablation compromised the functionality of ILC2s, resulting in a resolution of allergic airway inflammation. Notably, the different binding sites of BACH2 in ILC2s and T

Indexed as

Basic-Leucine Zipper Transcription FactorsImmunity, InnateLymphocytesAnimalsAsthmaCell DifferentiationEpigenesis, GeneticInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceMice, Inbred C57BLMice, KnockoutTh2 CellsBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsInterferon Regulatory Factor-4Interferon Regulatory Factors

Identifiers

PMID40749046
PMCPMC12315961

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.