Evidence map›Paper›PMID 29059238›Full record

ArticlePLoS pathogens2017

Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling.

Sudarshan Seshadri, David S J Allan, James R Carlyle, Lauren A Zenewicz

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  5. GPX4 restricts ferroptosis of NKp46Cell death & disease · 2024
    Article
  6. Article
  7. Review
  8. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Glucocorticoids Inhibit Group 3 Innate Lymphocyte IL-22 Production.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  17. 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

4 authors at 2 institutions in 2 countries.

Sudarshan SeshadriDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
David S J AllanDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada.
James R CarlyleDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada.
Lauren A ZenewiczDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.ORCID http://orcid.org/0000-0002-8787-5955
University of Oklahoma Health Sciences Center · USUniversity of Toronto · CA

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 2004 to 2023
$56.2M
Signaling by IgG receptors leading to phagocytosisR01AI049264 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI COGGESHALL, KENNETH MARK · 2002 to 2006
$1.6M
HSRD VA CDP 13-003NIAID NIH HHS R01 AI049264NIAID NIH HHS U19 AI062629
6 · The paper itself

Abstract

Bacillus anthracis, the causative agent of anthrax, secretes lethal toxin that down-regulates immune functions. Translocation of B. anthracis across mucosal epithelia is key for its dissemination and pathogenesis. Group 3 innate lymphocytes (ILC3s) are important in mucosal barrier maintenance due to their expression of the cytokine IL-22, a critical regulator of tissue responses and repair during homeostasis and inflammation. We found that B. anthracis lethal toxin perturbed ILC3 function in vitro and in vivo, revealing an unknown IL-23-mediated MAPK signaling pathway. Lethal toxin had no effects on the canonical STAT3-mediated IL-23 signaling pathway. Rather lethal toxin triggered the loss of several MAP2K kinases, which correlated with reduced activation of downstream ERK1/2 and p38, respectively. Inhibition studies showed the importance of MAPK signaling in IL-23-mediated production of IL-22. Our finding that MAPK signaling is required for optimal IL-22 production in ILC3s may lead to new approaches for targeting IL-22 biology.

Indexed as

AnimalsAnthraxAntigens, BacterialBacillus anthracisBacterial ToxinsHumansInterleukin-22Interleukin-23InterleukinsLymphocytesMAP Kinase Signaling SystemMiceVirulenceanthrax toxinAntigens, BacterialBacterial ToxinsInterleukin-22Interleukin-23Interleukins

Identifiers

PMID29059238
PMCPMC5695638
OpenAlexW2766860644

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.