Evidence map›Paper›PMID 37566453›Full record

ArticleeLife2023

TLR7 activation at epithelial barriers promotes emergency myelopoiesis and lung antiviral immunity.

William D Jackson, Chiara Giacomassi, Sophie Ward, Amber Owen, Tiago C Luis, Sarah Spear, Kevin J Woollard, Cecilia Johansson, Jessica Strid, Marina Botto

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  9. Article
  10. Unraveled role of TLR7-mediated interferon signaling activation in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  11. Review
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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

10 authors at 2 institutions in 2 countries.

William D Jackson *Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.
Chiara Giacomassi *Centre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.ORCID 0000-0003-0462-0381
Sophie WardCentre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.
Amber OwenNational Heart and Lung Institute, Imperial College London, London, United Kingdom.
Tiago C LuisCentre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.ORCID 0000-0002-6305-1257
Sarah SpearDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.ORCID 0000-0002-4306-3752
Kevin J WoollardCentre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.ORCID 0000-0002-9839-5463
Cecilia JohanssonNational Heart and Lung Institute, Imperial College London, London, United Kingdom.
Jessica StridCentre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.ORCID 0000-0003-3690-2201
Marina BottoCentre for Inflammatory Disease, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.ORCID 0000-0002-1458-3791
Imperial College London · GBLung Institute · US

Funding

Department of HealthWellcome TrustWellcome Trust 102126/B/13/ZWellcome Trust 108008/Z/15/ZWellcome Trust Institutional Strategic Support FundWellcome Trust Sir Henry Dale Fellowship - Wellcome Trust/Royal Society of Medicine 210424/Z/18/Z
6 · The paper itself

Abstract

Monocytes are heterogeneous innate effector leukocytes generated in the bone marrow and released into circulation in a CCR2-dependent manner. During infection or inflammation, myelopoiesis is modulated to rapidly meet the demand for more effector cells. Danger signals from peripheral tissues can influence this process. Herein we demonstrate that repetitive TLR7 stimulation via the epithelial barriers drove a potent emergency bone marrow monocyte response in mice. This process was unique to TLR7 activation and occurred independently of the canonical CCR2 and CX3CR1 axes or prototypical cytokines. The monocytes egressing the bone marrow had an immature Ly6C-high profile and differentiated into vascular Ly6C-low monocytes and tissue macrophages in multiple organs. They displayed a blunted cytokine response to further TLR7 stimulation and reduced lung viral load after RSV and influenza virus infection. These data provide insights into the emergency myelopoiesis likely to occur in response to the encounter of single-stranded RNA viruses at barrier sites.

Indexed as

MyelopoiesisToll-Like Receptor 7Virus DiseasesAnimalsCytokinesLungMembrane GlycoproteinsMiceMice, Inbred C57BLMonocytesCytokinesMembrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7haematopoiesisimmunologyinflammationmacrophagesmonocytesskinTLRvirusviruses

Identifiers

PMID37566453
PMCPMC10465127
OpenAlexW4385751090

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.