Evidence map›Paper›PMID 25921340›Full record

ArticleMucosal immunology2016

Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis.

L A Borthwick, L Barron, K M Hart, K M Vannella, R W Thompson, S Oland, A Cheever, J Sciurba, T R Ramalingam, A J Fisher and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
  2. Article
  3. The Role of Phagocytic Cells in the Achilles Tendon.International journal of molecular sciences · 2026
    Review
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  7. The immunology of asthma.Nature immunology · 2025
    Review
  8. Article
  9. Lung Immune Cell Niches and the Discovery of New Cell Subtypes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

27 more citing papers are in PubMed but not listed here.

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 at 4 institutions in 2 countries.

L A BorthwickTissue Fibrosis and Repair Group, Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle Upon Tyne, UK.
L BarronImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
K M HartImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
K M VannellaImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
R W ThompsonImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
S OlandImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
A CheeverImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
J SciurbaImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
T R RamalingamImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
A J FisherTissue Fibrosis and Repair Group, Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle Upon Tyne, UK.
T A WynnImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases · USFreeman Hospital · GBNational Institutes of Health · USNewcastle University · GB

Funding

Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
Immunological Intervention In SchistosomiasisZ01AI000829 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI WYNN, THOMAS · 1998 to 2008
$3.4M
Tissue Immunity and Repair ProgramZIAAI001194 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BELKAID, YASMINE · 2014 to 2015
$995k
Intramural NIH HHS Z01 AI000829
6 · The paper itself

Abstract

The roles of macrophages in type 2-driven inflammation and fibrosis remain unclear. Here, using CD11b-diphtheria toxin receptor (DTR) transgenic mice and three models of interleukin 13 (IL-13)-dependent inflammation, fibrosis, and immunity, we show that CD11b(+) F4/80(+) Ly6C(+) macrophages are required for the maintenance of type 2 immunity within affected tissues but not secondary lymphoid organs. Direct depletion of macrophages during the maintenance or resolution phases of secondary Schistosoma mansoni egg-induced granuloma formation caused a profound decrease in inflammation, fibrosis, and type 2 gene expression. Additional studies with CD11c-DTR and CD11b/CD11c-DTR double-transgenic mice suggested that macrophages but not dendritic cells were critical. Mechanistically, macrophage depletion impaired effector CD4(+) T helper type 2 (Th2) cell homing and activation within the inflamed lung. Depletion of CD11b(+) F4/80(+) Ly6C(+) macrophages similarly reduced house dust mite-induced allergic lung inflammation and suppressed IL-13-dependent immunity to the nematode parasite Nippostrongylus brasiliensis. Consequently, therapeutic strategies targeting macrophages offer a novel approach to ameliorate established type 2 inflammatory diseases.

Indexed as

AnimalsAntigens, DifferentiationAntigens, LyCD11b AntigenFibrosisGene Expression RegulationHeparin-binding EGF-like Growth FactorInterleukin-13LungMacrophages, AlveolarMiceMice, TransgenicNippostrongylusPneumoniaPyroglyphidaeSchistosoma mansoniAntigens, DifferentiationAntigens, LyCD11b AntigenHeparin-binding EGF-like Growth FactorInterleukin-13Ly-6C antigen, mousemonocyte-macrophage differentiation antigen

Identifiers

PMID25921340
PMCPMC4626445
OpenAlexW1989021802

What OpenQuestion holds

Textmetadata
LicenceTDM
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.