Evidence map›Paper›PMID 28779430›Full record

ArticleInflammopharmacology2018

Protective role of NKT cells and macrophage M2-driven phenotype in bleomycin-induced pulmonary fibrosis.

Felipe Grabarz, Cristhiane Favero Aguiar, Matheus Correa-Costa, Tárcio Teodoro Braga, Meire I Hyane, Vinícius Andrade-Oliveira, Maristella Almeida Landgraf, Niels Olsen Saraiva Câmara

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In one paragraph

Article in Inflammopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Macrophages and Pulmonary Fibrosis.Current molecular medicine · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023
    Review
  10. Article
  11. Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization.Tropical medicine and infectious disease · 2023
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

8 authors.

Felipe GrabarzLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.ORCID http://orcid.org/0000-0002-2002-9826
Cristhiane Favero AguiarLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.
Matheus Correa-CostaLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.
Tárcio Teodoro BragaLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.
Meire I HyaneLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.
Vinícius Andrade-OliveiraLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil.
Maristella Almeida LandgrafLaboratory of Hypertension, Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Niels Olsen Saraiva CâmaraLaboratory of Transplantation Immunobiology, Immunology Department, University of São Paulo, São Paulo, Brazil. niels@icb.usp.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is a result of an abnormal wound healing in lung tissue triggered by an excessive accumulation of extracellular matrix proteins, loss of tissue elasticity, and debit of ventilatory function. NKT cells are a major source of Th1 and Th2 cytokines and may be crucial in the polarization of M1/M2 macrophages in pulmonary fibrogenesis. Although there appears to be constant scientific progress in that field, pulmonary fibrosis still exhibits no current cure. From these facts, we hypothesized that NKT cells could influence the development of pulmonary fibrosis via modulation of macrophage activation. Wild type (WT) and NKT type I cell-deficient mice (Jα18

Indexed as

AnimalsBleomycinCollagenCytokinesDisease Models, AnimalGalactosylceramidesInflammationLungMacrophagesMiceMice, Inbred C57BLMice, KnockoutNatural Killer T-CellsPhenotypePulmonary FibrosisTh1 Cellsalpha-galactosylceramideBleomycinCollagenCytokinesGalactosylceramidesTransforming Growth Factor betaVimentinAlveolar macrophagesCytokineInflammationInterferon-gammaInterleukin-4Natural killer T cells

Identifiers

PMID28779430

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.