Evidence map›Paper›PMID 34797692›Full record

ArticleScience immunology2021

The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair.

Jack McCowan, Frédéric Fercoq, Phoebe M Kirkwood, Wouter T'Jonck, Lizi M Hegarty, Connar M Mawer, Richard Cunningham, Ananda S Mirchandani, Anna Hoy, Duncan C Humphries and 11 more

Abstract read
In one paragraph

Article in Science immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. EGR2 maintains neuropathic pain by promoting microglial phagocytosis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  17. mBio · 2025
    Article
  18. Review
  19. Article
  20. 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

21 authors.

Jack McCowanUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-5121-4549
Frédéric FercoqCancer Research UK Beatson Institute, Glasgow G61 1BD, UK.ORCID 0000-0002-4825-024X
Phoebe M KirkwoodUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-5245-718X
Wouter T'JonckUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-9390-525X
Lizi M HegartyUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-2127-5041
Connar M MawerUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.
Richard CunninghamUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0003-4127-8917
Ananda S MirchandaniUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.
Anna HoyUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-0632-6744
Duncan C HumphriesUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-5551-6536
Gareth-Rhys JonesUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0001-7355-2357
Carsten G HansenUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0003-0746-7482
Nik HiraniUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0001-8854-3605
Stephen J JenkinsUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0002-0233-5424
Sandrine HenriCentre d'Immunologie de Marseille-Luminy, Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280, 13288 Marseille, France.ORCID 0000-0002-8980-9193
Bernard MalissenCentre d'Immunologie de Marseille-Luminy, Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280, 13288 Marseille, France.ORCID 0000-0003-1340-9342
Sarah R WalmsleyUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0001-9584-174X
David H DockrellUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.
Philippa T K SaundersUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0001-9051-9380
Leo M CarlinCancer Research UK Beatson Institute, Glasgow G61 1BD, UK.ORCID 0000-0001-7172-5234
Calum C BainUniversity of Edinburgh Centre for Inflammation Research, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.ORCID 0000-0001-8884-327X

Funding

Biotechnology and Biological Sciences Research Council BB/J004243/1Cancer Research UK 23983Cancer Research UK A23983Cancer Research UK A31287Medical Research Council G0701740Medical Research Council MR/K001744/1Medical Research Council MR/K015206/1Medical Research Council MR/L008076/1Medical Research Council MR/M01245X/1Medical Research Council MR/N024524/1Medical Research Council MR/N02995X/1Wellcome Trust 110086/Z/15/ZWellcome Trust 206234Wellcome Trust 206234/Z/17/ZWellcome Trust 209220Wellcome Trust 209220/Z/17/ZWellcome Trust 220725Wellcome Trust 220725/Z/20/Z
6 · The paper itself

Abstract

Alveolar macrophages are the most abundant macrophages in the healthy lung where they play key roles in homeostasis and immune surveillance against airborne pathogens. Tissue-specific differentiation and survival of alveolar macrophages rely on niche-derived factors, such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor–β (TGF-β). However, the nature of the downstream molecular pathways that regulate the identity and function of alveolar macrophages and their response to injury remain poorly understood. Here, we identify that the transcription factor EGR2 is an evolutionarily conserved feature of lung alveolar macrophages and show that cell-intrinsic EGR2 is indispensable for the tissue-specific identity of alveolar macrophages. Mechanistically, we show that EGR2 is driven by TGF-β and GM-CSF in a PPAR-γ–dependent manner to control alveolar macrophage differentiation. Functionally, EGR2 was dispensable for the regulation of lipids in the airways but crucial for the effective handling of the respiratory pathogen

Indexed as

AnimalsEarly Growth Response Protein 2FemaleHumansMacrophages, AlveolarMaleMicePneumococcal InfectionsStreptococcus pneumoniaeEarly Growth Response Protein 2EGR2 protein, humanEgr2 protein, mouse

Identifiers

PMID34797692
PMCPMC7612216

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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.