Evidence map›Paper›PMID 33211671›Full record

ArticleThe Journal of clinical investigation2021

Extracellular traps released by antimicrobial TH17 cells contribute to host defense.

George W Agak, Alice Mouton, Rosane Mb Teles, Thomas Weston, Marco Morselli, Priscila R Andrade, Matteo Pellegrini, Robert L Modlin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Characterization of an isogenicInfection and immunity · 2026
    Article
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  13. Frontiers in immunology · 2024
    Article
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  17. Review
  18. Review
  19. Article
  20. A narrative review of research progress on the role ofAnnals of translational medicine · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

George W AgakDivision of Dermatology, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Alice MoutonDepartment of Ecology and Evolutionary Biology, UCLA, Los Angeles, California, USA.
Rosane Mb TelesDivision of Dermatology, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Thomas WestonDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Marco MorselliDepartment of Molecular, Cell and Developmental Biology, and.
Priscila R AndradeDivision of Dermatology, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Matteo PellegriniDepartment of Molecular, Cell and Developmental Biology, and.
Robert L ModlinDivision of Dermatology, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
University of California, Los Angeles · USQuantitative BioSciences · US

Funding

Molecular Analysis of the Host Immune Response in LeprosyR01AI022553 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROBERT L MODLIN · 1989 to 2026
$15.7M
TCR GAMMA/DELTA LYMPHOCYTES IN HUMAN SKIN LESIONSR01AR040312 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MODLIN, ROBERT L · 1990 to 2025
$10.4M
The skin microbiome in acneR01AR074302 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GALLO, RICHARD L, MODLIN, ROBERT L · 2018 to 2022
$2.6M
IL-26 in host defense against infection by intracellular bacteria in skinR01AR073252 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODLIN, ROBERT L · 2019 to 2023
$2.1M
The nature of Propionibacterium acnes-induced inflammatory immune responses in acne vulgarisK01AR071479 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AGAK, GEORGE W · 2017 to 2022
$958k
Multiphoton Microscope for Deep Tissue ImagingS10OD025017 · OD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BENTOLILA, LAURENT A. · 2018 to 2018
$599k
NIAID NIH HHS R01 AI022553NIAMS NIH HHS K01 AR071479NIAMS NIH HHS R01 AR040312NIAMS NIH HHS R01 AR073252NIAMS NIH HHS R01 AR074302NIH HHS S10 OD025017
6 · The paper itself

Abstract

TH17 cell subpopulations have been defined that contribute to inflammation and homeostasis, yet the characteristics of TH17 cells that contribute to host defense against infection are not clear. To elucidate the antimicrobial machinery of the TH17 subset, we studied the response to Cutibacterium acnes, a skin commensal that is resistant to IL-26, the only known TH17-secreted protein with direct antimicrobial activity. We generated C. acnes-specific antimicrobial TH17 clones (AMTH17) with varying antimicrobial activity against C. acnes, which we correlated by RNA sequencing to the expression of transcripts encoding proteins that contribute to antimicrobial activity. Additionally, we validated that AMTH17-mediated killing of C. acnes and bacterial pathogens was dependent on the secretion of granulysin, granzyme B, perforin, and histone H2B. We found that AMTH17 cells can release fibrous structures composed of DNA decorated with histone H2B that entangle C. acnes that we call T cell extracellular traps (TETs). Within acne lesions, H2B and IL-17 colocalized in CD4+ T cells, in proximity to TETs in the extracellular space composed of DNA decorated with H2B. This study identifies a functionally distinct subpopulation of TH17 cells with an ability to form TETs containing secreted antimicrobial proteins that capture and kill bacteria.

Indexed as

Acne VulgarisExtracellular TrapsHumansPropionibacteriaceaeRNA-SeqSkin Diseases, BacterialTh17 CellsImmunologyT cells

Identifiers

PMID33211671
PMCPMC7810473
OpenAlexW3106441865

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.