Evidence map›Paper›PMID 29907868›Full record

ArticleMucosal immunology2018

T cell-directed IL-17 production by lung granular γδ T cells is coordinated by a novel IL-2 and IL-1β circuit.

Antoine Ménoret, James A Buturla, Maria M Xu, Julia Svedova, Sanjeev Kumar, Vijay A K Rathinam, Anthony T Vella

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Development of γδ T Cells: Soldiers on the Front Lines of Immune Battles.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. 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

7 authors at 2 institutions in 1 country.

Antoine MénoretDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA. menoret@uchc.edu.
James A ButurlaDepartment of Internal Medicine, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA.
Maria M XuDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA.
Julia SvedovaDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA.
Sanjeev KumarDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA.
Vijay A K RathinamDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA.
Anthony T VellaDepartment of Immunology, UConn Health, 263 Farmington Avenue, Farmington, CT, 06030, USA. vella@uchc.edu.
UConn Health · USUniversity of Connecticut · US

Funding

Sustained adaptive immunity in the mucosaP01AI056172 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T · 2003 to 2017
$22.3M
NIAID NIH HHS P01 AI056172
6 · The paper itself

Abstract

Immune-mediated lung is considered the result of an exacerbated innate injury immune response, although a role for adaptive lymphocytes is emerging. αβ T cells specific for S. aureus enterotoxin A orchestrate a Tγδ17 response during lung injury. However, the mechanism driving IL-17 production is unclear. Here, we show a role for IL-2 triggering IL-17 production by lung granular γδ T cells as IL-17 synthesis and neutrophil recruitment was reduced by IL-2 blocking mAbs in vitro and in vivo. Mass cytometry analysis revealed that lung γδ T cells responded directly to IL-2 as evident from STAT5 phosphorylation and RoRγt expression. IL-2 receptor blocking mAbs and JAK inhibition impaired STAT5 phosphorylation and IL-17 release. Moreover, inhalation of S. aureus enterotoxin A induced IL-2 secretion and caspase-1-dependent IL-1β activation to drive IL-17 production. This T-cell-mediated inflammasome-dependent IL-17 response is maximum when lung Tγδ17 cells were sequentially stimulated first with IL-2 then IL-1β. Interestingly, when IL-2 is given therapeutically to cancer patients it carries a known risk of lung injury that is largely indistinguishable from that seen in sepsis. Hence, this novel mechanism reveals therapeutic targets treating both acute lung injury and high-dose IL-2 toxicity in cancer.

Indexed as

AnimalsAntibodies, MonoclonalCaspase 1Interleukin-17Interleukin-1betaInterleukin-2Janus KinasesLungMiceMice, Inbred C57BLNeutrophilsNuclear Receptor Subfamily 1, Group F, Member 3PhosphorylationSaccharomyces cerevisiaeSTAT5 Transcription FactorT-LymphocytesAntibodies, MonoclonalCaspase 1Interleukin-17Interleukin-1betaInterleukin-2Janus KinasesNuclear Receptor Subfamily 1, Group F, Member 3STAT5 Transcription Factor

Identifiers

PMID29907868
PMCPMC6668340
OpenAlexW2808293247

What OpenQuestion holds

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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.