Evidence map›Paper›PMID 35263568›Full record

ArticleImmunity2022

A nonredundant role for T cell-derived interleukin 22 in antibacterial defense of colonic crypts.

Carlene L Zindl, Steven J Witte, Vincent A Laufer, Min Gao, Zongliang Yue, Karen M Janowski, Baiyi Cai, Blake F Frey, Daniel J Silberger, Stacey N Harbour and 9 more

Open access · greenAbstract read
In one paragraph

Article in Immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Rehydration rescues Il22Nature communications · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Virulence · 2024
    Article
  20. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    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

19 authors at 2 institutions in 2 countries.

Carlene L ZindlDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: carlenezindl@uabmc.edu.
Steven J WitteDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Vincent A LauferDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Min GaoDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Informatics Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Zongliang YueDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Informatics Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Karen M JanowskiDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Baiyi CaiDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Blake F FreyDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Daniel J SilbergerDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Stacey N HarbourDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Jeffrey R SingerDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Henrietta TurnerDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Frances E LundDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Bruce A VallanceDepartment of Pediatrics, University of British Columbia, Vancouver, BC V6H 3V4, Canada.
Alexander F RosenbergInformatics Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Trenton R SchoebDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Jake Y ChenDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Informatics Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Robin D HattonDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Casey T WeaverDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: cweaver@uab.edu.
University of Alabama at Birmingham · USUniversity of British Columbia · CA

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Coordination of Innate and Adaptive Immunity in Intestinal Barrier DefenseR37AI169864 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Casey T Weaver · 2022 to 2026
$2.8M
Training Program in Rheumatic and Musculoskeletal Diseases ResearchT32AR069516 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI John D Mountz · 2016 to 2026
$2.6M
Specialization of Innate and Adaptive Immune Cells in Intestinal Barrier FunctionR01DK113789 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WEAVER, CASEY T · 2017 to 2021
$2.3M
Role of Rorγt positive Innate Lymphoid Cells in Neonatal Intestinal Barrier DevelopmentF30DK105680 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SINGER, JEFFREY ROBERT · 2015 to 2018
$154k
NCI NIH HHS P30 CA013148NIAID NIH HHS R37 AI169864NIAMS NIH HHS T32 AR069516NIDDK NIH HHS F30 DK105680NIDDK NIH HHS R01 DK113789
6 · The paper itself

Abstract

Interleukin (IL)-22 is central to immune defense at barrier sites. We examined the contributions of innate lymphoid cell (ILC) and T cell-derived IL-22 during Citrobacter rodentium (C.r) infection using mice that both report Il22 expression and allow lineage-specific deletion. ILC-derived IL-22 activated STAT3 in C.r-colonized surface intestinal epithelial cells (IECs) but only temporally restrained bacterial growth. T cell-derived IL-22 induced a more robust and extensive activation of STAT3 in IECs, including IECs lining colonic crypts, and T cell-specific deficiency of IL-22 led to pathogen invasion of the crypts and increased mortality. This reflected a requirement for T cell-derived IL-22 for the expression of a host-protective transcriptomic program that included AMPs, neutrophil-recruiting chemokines, and mucin-related molecules, and it restricted IFNγ-induced proinflammatory genes. Our findings demonstrate spatiotemporal differences in the production and action of IL-22 by ILCs and T cells during infection and reveal an indispensable role for IL-22-producing T cells in the protection of the intestinal crypts.

Indexed as

Citrobacter rodentiumEnterobacteriaceae InfectionsAnimalsAnti-Bacterial AgentsImmunity, InnateInterleukin-22InterleukinsIntestinal MucosaLymphocytesMiceMice, Inbred C57BLT-LymphocytesAnti-Bacterial AgentsInterleukin-22InterleukinsAMPsCD4 T cellschemokinesCitrobacter rodentiumcolonic crypt IECscolonic surface IECsIFNγIL-22innate cellsmucinsTNF

Identifiers

PMID35263568
PMCPMC9126440
OpenAlexW4220704062

What OpenQuestion holds

Textmetadata
LicenceTDM
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.