Evidence map›Paper›PMID 30984202›Full record

ArticleFrontiers in immunology2019

Commensal and Pathogenic Bacteria Indirectly Induce IL-22 but Not IFNγ Production From Human Colonic ILC3s via Multiple Mechanisms.

Moriah J Castleman, Stephanie M Dillon, Christine M Purba, Andrew C Cogswell, Jon J Kibbie, Martin D McCarter, Mario L Santiago, Edward Barker, Cara C Wilson

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-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

45 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  6. Intestinal IL-22RA1 signaling regulatesFrontiers in microbiology · 2025
    Article
  7. Article
  8. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. mBio · 2024
    Article
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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

9 authors at 2 institutions in 1 country.

Moriah J CastlemanDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
Stephanie M DillonDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
Christine M PurbaDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
Andrew C CogswellDepartment of Microbial Pathogens and Immunity, Rush University Medical Center, Chicago, IL, United States.
Jon J KibbieDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
Martin D McCarterDepartment of Surgery, University of Colorado Anschutz Medical, Aurora, CO, United States.
Mario L SantiagoDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
Edward BarkerDepartment of Microbial Pathogens and Immunity, Rush University Medical Center, Chicago, IL, United States.
Cara C WilsonDivision of Infectious Disease, Department of Medicine, University of Colorado Anschutz Medical, Aurora, CO, United States.
University of Colorado Anschutz Medical Campus · USRush University Medical Center · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Medical Scientist Training ProgramT32GM008497 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI WILSON, CARA C. · 1993 to 2022
$15.2M
TRAINING PROGRAM IN IMMUNOLOGYT32AI007405 · NIAID · UNIVERSITY OF COLORADO DENVER · PI Laurel L Lenz, Raul Martin Torres · 1991 to 2026
$10.5M
Switch from homeostatic to inflammatory cytokines by NK/ILC in HIV-infected gutR01AI118983 · NIAID · RUSH UNIVERSITY MEDICAL CENTER · PI BARKER, EDWARD, WILSON, CARA C. · 2015 to 2019
$2.7M
NCI NIH HHS P30 CA046934NIAID NIH HHS R01 AI118983NIAID NIH HHS T32 AI007405NIGMS NIH HHS T32 GM008497
6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) are a diverse family of cells that play critical roles in mucosal immunity. One subset of the ILC family, Group 3 ILCs (ILC3s), has been shown to aid in gut homeostasis through the production of IL-22. IL-22 promotes gut homeostasis through its functional effect on the epithelial barrier. When gut epithelial barrier integrity is compromised, such as in Human Immunodeficiency Virus (HIV) infection and inflammatory bowel disease (IBD), microbes from the gut lumen translocate into the lamina propria, inducing a multitude of potentially pathogenic immune responses. In murine models of bacterial infection, there is evidence that bacteria can induce pro-inflammatory IFNγ production in ILC3s. However, the impact of diverse translocating bacteria, particularly commensal bacteria, in dictating IFNγ versus IL-22 production by human gut ILC3s remains unclear. Here, we utilized an

Indexed as

ColonImmunity, InnateIntestinal MucosaBacterial TranslocationGastrointestinal MicrobiomeGram-Negative BacteriaGram-Positive BacteriaHumansInterferon-gammaInterleukin-1betaInterleukin-22InterleukinsLymphocytesIFNG protein, humanIL1B protein, humanInterferon-gammaInterleukin-1betaInterleukin-22Interleukinscolonic mucosacommensal bacteriahumanIL-1βIL-23innate lymphoid cellsmyeloid dendritic cellsNKp44

Identifiers

PMID30984202
PMCPMC6450192
OpenAlexW2933593704

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.