Evidence map›Paper›PMID 21356368›Full record

ArticleThe American journal of pathology2011

γδ T cells attenuate bleomycin-induced fibrosis through the production of CXCL10.

Derek A Pociask, Kong Chen, Sun Mi Choi, Tim D Oury, Chad Steele, Jay K Kolls

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

  1. How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026
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  16. The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023
    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

6 authors at 3 institutions in 1 country.

Derek A PociaskDepartment of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA. dpocia@lsuhsc.edu
Kong Chen
Sun Mi Choi
Tim D Oury
Chad Steele
Jay K Kolls
Louisiana State University Health Sciences Center New Orleans · USUniversity of Alabama at Birmingham · USUniversity of Pittsburgh · US

Funding

IL-23 / Il-17 and Lung Host DefenseR01HL079142 · NHLBI · LSU HEALTH SCIENCES CENTER · PI KOLLS, JAY K · 2005 to 2009
$1.9M
NHLBI NIH HHS R01 HL079142NHLBI NIH HHS R01-HL079142
6 · The paper itself

Abstract

γδ T cells are a subset of T cells associated with epithelial mucosal tissues and play a prominent role in both promoting and dampening inflammatory responses to pathogens; in addition, they strongly mediate epithelial repair. By using a bleomycin model of pulmonary fibrosis, we found that γδ T-cell populations dramatically increased after bleomycin administration. To determine the importance of these cells, we exposed mice lacking the δ chain of the γδ T-cell receptor (γδ knockout [KO]) to bleomycin. Pulmonary fibrosis was more severe in γδ KO mice, as measured by collagen deposition (hydroxyproline) and histopathological features. Furthermore, there was no evidence of resolution of the fibrotic response up to 45 days after bleomycin therapy. In contrast to control mice, γδ KO mice had decreased concentrations of IL-6, granulocyte colony stimulating factor, chemokine CXC ligand (CXCL) 1, and interferon inducible protein 10/CXCL10. In vitro culture of γδ T cells purified from lungs 17 days after bleomycin exposure (a time of peak influx of these cells) demonstrated that γδ T cells produced substantial quantities of all four of these cytokines, suggesting that γδ T cells are a predominant source of these proteins. To demonstrate that γδ T cells are effector cells in the fibrotic response, we performed adoptive transfer experiments with γδ T cells sorted from bleomycin-treated lungs; these cells were sufficient to resolve fibrosis in γδ KO mice and restore CXCL10 levels comparable to wild-type mice. Furthermore, overexpression of CXCL10 in the lung decreased the severity of fibrosis seen in the γδ KO mice. Finally, adoptive transfer of γδ T cells from CXCL10(-/-) mice failed to reverse the severe fibrosis in γδ KO mice. These results indicate that γδ T cells promote the resolution of fibrosis through the production of CXCL10.

Indexed as

AdenoviridaeAdoptive TransferAnimalsBleomycinChemokine CXCL1Chemokine CXCL10CollagenInflammationInterleukin-6LungMiceMice, Inbred C57BLMice, KnockoutPulmonary FibrosisReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesBleomycinChemokine CXCL1Chemokine CXCL10CollagenCxcl10 protein, mouseCxcl1 protein, mouseInterleukin-6Receptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID21356368
PMCPMC3070585
OpenAlexW2015047621

What OpenQuestion holds

Textmetadata
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.