Evidence map›Paper›PMID 32033836›Full record

ArticleJournal of autoimmunity2020

Tissue alarmins and adaptive cytokine induce dynamic and distinct transcriptional responses in tissue-resident intraepithelial cytotoxic T lymphocytes.

Maria Magdalena Zorro, Raul Aguirre-Gamboa, Toufic Mayassi, Cezary Ciszewski, Donatella Barisani, Shixian Hu, Rinse K Weersma, Sebo Withoff, Yang Li, Cisca Wijmenga and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of autoimmunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Celiac disease: From genetics to epigenetics.World journal of gastroenterology · 2022
    Review
  3. Review
  4. Adoptive T-cell Immunotherapy: Perfecting Self-Defenses.Experientia supplementum (2012) · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
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

12 authors at 4 institutions in 5 countries.

Maria Magdalena ZorroDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Raul Aguirre-GamboaDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Toufic MayassiDepartment of Medicine, University of Chicago, Chicago, USA; Committee on Immunology, University of Chicago, Chicago, USA.
Cezary CiszewskiDepartment of Medicine, University of Chicago, Chicago, USA.
Donatella BarisaniSchool of Medicine and Surgery, University of Milano-Bicocca, Italy.
Shixian HuDepartment of Gastroenterology and Hepatology, University Medical Center, Groningen, University of Groningen, Groningen, the Netherlands.
Rinse K WeersmaDepartment of Gastroenterology and Hepatology, University Medical Center, Groningen, University of Groningen, Groningen, the Netherlands.
Sebo WithoffDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Yang LiDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Department of Internal Medicine and Radboud Center for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, the Netherlands; Department of Computational Biology for Individualised Infection Medicine, Centre for Individualised Infection Medicine, Helmholtz Centre for Infection Research, Hannover Medical School. Hannover, Germany.
Cisca WijmengaDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Oslo, Norway.
Bana JabriDepartment of Medicine, University of Chicago, Chicago, USA; Committee on Immunology, University of Chicago, Chicago, USA. Electronic address: bjabri@bsd.uchicago.edu.
Iris H JonkersDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Oslo, Norway. Electronic address: i.h.jonkers@umcg.nl.
University of Groningen · NLUniversity Medical Center Groningen · NLUniversity of Chicago · USUniversity of Milano-Bicocca · IT

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI LIU, CAMBRIAN YANGSHAO · 1990 to 2025
$29.8M
INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007090 · NIAID · UNIVERSITY OF CHICAGO · PI Peter Aidan Savage · 1985 to 2026
$11.7M
Innate and adaptive immunity in celiac diseaseR01DK067180 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2005 to 2024
$8.5M
Viral infections and celiac disease pathogenesisR01DK098435 · NIDDK · UNIVERSITY OF CHICAGO · PI DERMODY, TERENCE S., JABRI, BANA · 2014 to 2022
$5.4M
NCI NIH HHS P30 CA014599NIAID NIH HHS T32 AI007090NIDDK NIH HHS P30 DK042086NIDDK NIH HHS R01 DK067180NIDDK NIH HHS R01 DK098435
6 · The paper itself

Abstract

The respective effects of tissue alarmins interleukin (IL)-15 and interferon beta (IFNβ), and IL-21 produced by T cells on the reprogramming of cytotoxic T lymphocytes (CTLs) that cause tissue destruction in celiac disease is poorly understood. Transcriptomic and epigenetic profiling of primary intestinal CTLs showed massive and distinct temporal transcriptional changes in response to tissue alarmins, while the impact of IL-21 was limited. Only anti-viral pathways were induced in response to all the three stimuli, albeit with differences in dynamics and strength. Moreover, changes in gene expression were primarily independent of changes in H3K27ac, suggesting that other regulatory mechanisms drive the robust transcriptional response. Finally, we found that IL-15/IFNβ/IL-21 transcriptional signatures could be linked to transcriptional alterations in risk loci for complex immune diseases. Together these results provide new insights into molecular mechanisms that fuel the activation of CTLs under conditions that emulate the inflammatory environment in patients with autoimmune diseases.

Indexed as

Gene Expression RegulationAlarminsAutoimmunityCeliac DiseaseCytokinesGene Expression ProfilingHumansInflammatory Bowel DiseasesInterleukin-15Intestinal MucosaIntraepithelial LymphocytesPromoter Regions, GeneticT-Lymphocytes, CytotoxicAlarminsCytokinesIL15 protein, humanInterleukin-15Autoimmune diseaseCytotoxic T lymphocytesIFNβIL-15IL-21Intraepithelial lymphocytesTissue-resident lymphocytes

Identifiers

PMID32033836
PMCPMC7049906
OpenAlexW3005010291

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.