Evidence map›Paper›PMID 32515782›Full record

ArticleThe Journal of experimental medicine2020

BACH2 drives quiescence and maintenance of resting Treg cells to promote homeostasis and cancer immunosuppression.

Francis M Grant, Jie Yang, Rabab Nasrallah, James Clarke, Firas Sadiyah, Sarah K Whiteside, Charlotte J Imianowski, Paula Kuo, Panagiota Vardaka, Tihomir Todorov and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  11. IL-27 promotes Treg cell expression of CD122 and fitness at homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  18. An integrated transcription factor framework for Treg identity and diversity.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

18 authors at 6 institutions in 3 countries.

Francis M GrantLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Jie YangLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Rabab NasrallahLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
James ClarkeLa Jolla Institute for Allergy and Immunology, La Jolla, CA.
Firas SadiyahLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Sarah K WhitesideLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Charlotte J ImianowskiLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Paula KuoLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Panagiota VardakaLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Tihomir TodorovLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Nordin ZandhuisLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Ilinca PatrascanLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
David F ToughEpigenetics DPU, Immunoinflammation Therapeutic Area Unit, GSK Medicines Research Centre, Stevenage, UK.
Kohei KometaniLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Robert EilOregon Health and Science University School of Medicine, Portland, OR.
Tomohiro KurosakiLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Klaus OkkenhaugDepartment of Pathology, University of Cambridge, Cambridge, UK.
Rahul RoychoudhuriLaboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
Babraham Institute · GBRIKEN Center for Integrative Medical Sciences · JPAge UK · GBLa Jolla Institute for Immunology · USOregon Health & Science University · USUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/N007794/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Biotechnology and Biological Sciences Research Council BBS/E/B/000C0409Biotechnology and Biological Sciences Research Council BBS/E/B/000C0427Biotechnology and Biological Sciences Research Council BBS/E/B/000C0428Cancer Research UK 22597Cancer Research UK C52623/A22597Medical Research Council MR/S024468/1Medical Research Council MR/S024468/2Wellcome TrustWellcome Trust 105663/Z/14/Z
6 · The paper itself

Abstract

Regulatory T (Treg) cell populations are composed of functionally quiescent resting Treg (rTreg) cells which differentiate into activated Treg (aTreg) cells upon antigen stimulation. How rTreg cells remain quiescent despite chronic exposure to cognate self- and foreign antigens is unclear. The transcription factor BACH2 is critical for early Treg lineage specification, but its function following lineage commitment is unresolved. Here, we show that BACH2 is repurposed following Treg lineage commitment and promotes the quiescence and long-term maintenance of rTreg cells. Bach2 is highly expressed in rTreg cells but is down-regulated in aTreg cells and during inflammation. In rTreg cells, BACH2 binds to enhancers of genes involved in aTreg differentiation and represses their TCR-driven induction by competing with AP-1 factors for DNA binding. This function promotes rTreg cell quiescence and long-term maintenance and is required for immune homeostasis and durable immunosuppression in cancer. Thus, BACH2 supports a "division of labor" between quiescent rTreg cells and their activated progeny in Treg maintenance and function, respectively.

Indexed as

Cell CycleHomeostasisImmunosuppression TherapyAnimalsBasic-Leucine Zipper Transcription FactorsCell DifferentiationCell LineageCell Line, TumorCytokinesDown-RegulationForkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansInflammationIntegrasesMice, Inbred C57BLBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsCre recombinaseCytokinesForkhead Transcription FactorsFoxp3 protein, mouseIntegrasesReceptors, Antigen, T-CellTranscription Factor AP-1

Identifiers

PMID32515782
PMCPMC7478731
OpenAlexW3034038263

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.