Evidence map›Paper›PMID 27083148›Full record

ArticleClinical and experimental immunology2016

The regulatory role of interferon-γ producing gamma delta T cells via the suppression of T helper 17 cell activity in bleomycin-induced pulmonary fibrosis.

S Segawa, D Goto, A Iizuka, S Kaneko, M Yokosawa, Y Kondo, I Matsumoto, T Sumida

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. CD4Frontiers in immunology · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Roles of Immune Cells in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2020
    Review
  18. T Cells in Fibrosis and Fibrotic Diseases.Frontiers in immunology · 2020
    Review
  19. Th17 cells contribute to pulmonary fibrosis and inflammation during chronic kidney disease progression after acute ischemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  20. Association of Decreased Percentage of Vδ2Frontiers in immunology · 2018
    Article
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 at 1 institution in 1 country.

S SegawaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
D GotoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
A IizukaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
S KanekoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
M YokosawaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Y KondoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
I MatsumotoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
T SumidaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interstitial pneumonia (IP) is a chronic progressive interstitial lung disease associated with poor prognosis and high mortality. However, the pathogenesis of IP remains to be elucidated. The aim of this study was to clarify the role of pulmonary γδT cells in IP. In wild-type (WT) mice exposed to bleomycin, pulmonary γδT cells were expanded and produced large amounts of interferon (IFN)-γ and interleukin (IL)-17A. Histological and biochemical analyses showed that bleomycin-induced IP was more severe in T cell receptor (TCR-δ-deficient (TCRδ(-/-) ) mice than WT mice. In TCRδ(-/-) mice, pulmonary IL-17A(+) CD4(+) Τ cells expanded at days 7 and 14 after bleomycin exposure. In TCRδ(-/-) mice infused with γδT cells from WT mice, the number of pulmonary IL-17A(+) CD4(+) T cells was lower than in TCRδ(-/-) mice. The examination of IL-17A(-/-) TCRδ(-/-) mice indicated that γδT cells suppressed pulmonary fibrosis through the suppression of IL-17A(+) CD4(+) T cells. The differentiation of T helper (Th)17 cells was determined in vitro, and CD4(+) cells isolated from TCRδ(-/-) mice showed normal differentiation of Th17 cells compared with WT mice. Th17 cell differentiation was suppressed in the presence of IFN-γ producing γδT cells in vitro. Pulmonary fibrosis was attenuated by IFN-γ-producing γδT cells through the suppression of pulmonary IL-17A(+) CD4(+) T cells. These results suggested that pulmonary γδT cells seem to play a regulatory role in the development of bleomycin-induced IP mouse model via the suppression of IL-17A production.

Indexed as

AnimalsBleomycinCD4-Positive T-LymphocytesCell DifferentiationDisease Models, AnimalInterferon-gammaInterleukin-17LungLung Diseases, InterstitialMiceMice, Inbred C57BLMice, KnockoutPulmonary FibrosisReceptors, Antigen, T-Cell, gamma-deltaTh17 CellsT-LymphocytesBleomycinIl17a protein, mouseInterferon-gammaInterleukin-17Receptors, Antigen, T-Cell, gamma-deltagamma delta T cellIL-17Ainterferon-γinterstitial pneumonia

Identifiers

PMID27083148
PMCPMC4991517
OpenAlexW2343112685

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.