Evidence map›Paper›PMID 36070768›Full record

ArticleImmunity2022

Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling.

Mathias Pawlak, David DeTomaso, Alexandra Schnell, Gerd Meyer Zu Horste, Youjin Lee, Jackson Nyman, Danielle Dionne, Brianna M L Regan, Vasundhara Singh, Toni Delorey and 10 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Dissecting PGENature communications · 2026
    Article
  4. Review
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  16. Article
  17. Macrophage Functions in Psoriasis: Lessons from Mouse Models.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Review
  20. Precision medicine in inflammatory bowel disease.Precision clinical medicine · 2023
    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

20 authors at 6 institutions in 2 countries.

Mathias PawlakEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
David DeTomasoDepartment of Electrical Engineering and Computer Sciences and Center for Computational Biology, UC Berkeley, Berkeley, CA 94720, USA.
Alexandra SchnellEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Gerd Meyer Zu HorsteEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Youjin LeeEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Jackson NymanKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Danielle DionneKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Brianna M L ReganEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Vasundhara SinghKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Toni DeloreyKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Markus A SchrammEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Chao WangEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Antonia WallrappEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Patrick R BurkettEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Samantha J RiesenfeldEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Ana C AndersonEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Aviv RegevKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Ramnik J XavierKlarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Molecular Biology, MGH, Boston, MA 02114, USA. Electronic address: rxavier@broadinstitute.org.
Nir YosefDepartment of Electrical Engineering and Computer Sciences and Center for Computational Biology, UC Berkeley, Berkeley, CA 94720, USA; Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel; Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA. Electronic address: niryosef@eecs.berkeley.edu.
Vijay K KuchrooEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: vkuchroo@rics.bwh.harvard.edu.
Broad Institute · USBrigham and Women's Hospital · USHarvard University · USMassachusetts Institute of Technology · USUniversity of California, Berkeley · USWeizmann Institute of Science · IL

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7M
Transgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SHARPE, ARLENE H. · 2003 to 2023
$42.5M
Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Transgenic / Knock-out mouse coreP01AI073748 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2008 to 2019
$17.1M
Project 2: Genes required for dendritic cell responses to pathogens and T cellsU19AI133524 · NIAID · HARVARD MEDICAL SCHOOL · PI SHARPE, ARLENE H. · 2017 to 2021
$12.3M
Role of Tim-3:Bat-3 pathway in inducing tolerogenic DCs and peripheral toleranceR01AI144166 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI VIJAY K. KUCHROO · 2020 to 2026
$3.2M
NIAID NIH HHS P01 AI039671NIAID NIH HHS P01 AI056299NIAID NIH HHS P01 AI073748NIAID NIH HHS R01 AI144166NIAID NIH HHS U19 AI133524NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Interleukin-23 receptor plays a critical role in inducing inflammation and autoimmunity. Here, we report that Th1-like cells differentiated in vitro with IL-12 + IL-21 showed similar IL-23R expression to that of pathogenic Th17 cells using eGFP reporter mice. Fate mapping established that these cells did not transition through a Th17 cell state prior to becoming Th1-like cells, and we observed their emergence in vivo in the T cell adoptive transfer colitis model. Using IL-23R-deficient Th1-like cells, we demonstrated that IL-23R was required for the development of a highly colitogenic phenotype. Single-cell RNA sequencing analysis of intestinal T cells identified IL-23R-dependent genes in Th1-like cells that differed from those expressed in Th17 cells. The perturbation of one of these regulators (CD160) in Th1-like cells inhibited the induction of colitis. We thus uncouple IL-23R as a purely Th17 cell-specific factor and implicate IL-23R signaling as a pathogenic driver in Th1-like cells inducing tissue inflammation.

Indexed as

ColitisReceptors, InterleukinAnimalsInflammationInterleukin-23MiceMice, Inbred C57BLPhenotypeTh17 CellsTh1 CellsInterleukin-23Receptors, InterleukinautoimmunitycolitisIL-23IL-23 receptorinflammationinflammatory bowel diseasepre-clinical mouse modelsingle-cell RNA sequencingTh1-like cellT helper cell

Identifiers

PMID36070768
PMCPMC9808605
OpenAlexW4294770778

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.