Evidence map›Paper›PMID 30145369›Full record

ArticleCytokine2018

Interleukin 33 regulates gene expression in intestinal epithelial cells independently of its nuclear localization.

Zhengxiang He, Lili Chen, Glaucia C Furtado, Sergio A Lira

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2018. 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 31% 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, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. IL-33 mediates Pseudomonas induced airway fibrogenesis and is associated with CLAD.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023
    Article
  7. Article
  8. IFN-γCellular & molecular immunology · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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 1 institution in 1 country.

Zhengxiang HePrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Lili ChenPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Glaucia C FurtadoPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Sergio A LiraPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States. Electronic address: sergio.lira@mssm.edu.
Icahn School of Medicine at Mount Sinai · US

Funding

THE ROLE OF ICSBP IN MUCOSAL IMMUNE RESPONSEP01DK072201 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HARPAZ, NOAM · 2006 to 2015
$14.6M
Mechanisms associated with flares and remission in colitisR01DK110352 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2017 to 2025
$5.1M
Molecular pathogenesis of intestinal serrated polypsR01CA161373 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2011 to 2020
$3.7M
NCI NIH HHS R01 CA161373NIDDK NIH HHS P01 DK072201NIDDK NIH HHS R01 DK110352
6 · The paper itself

Abstract

Interleukin 33 (IL33) is a cytokine found in the extracellular space (mature IL33) or in the cell nucleus (full-length IL33). Nuclear accumulation of IL33 has been reported in intestinal epithelial cells (IEC) during intestinal inflammation and cancer, but a functional role for this nuclear form remains unclear. To study the role of nuclear IL33 in IEC, we generated transgenic mice expressing full-length IL33 in the intestinal epithelium (Vfl33 mice). Expression of full-length IL33 in the epithelium resulted in accumulation of IL33 protein in the nucleus and secretion of IL33. Over-expression of full-length IL33 by IEC did not promote gut inflammation, but induced expression of genes in the IEC and lamina propria lymphocytes (LPL) that correlated negatively with genes expressed in inflammatory bowel diseases (IBD). Because the IL33 receptor ST2 is expressed by IEC, there was the potential that both the mature and full-length forms could mediate this effect. To specifically interrogate the transcriptional role of nuclear IL33, we intercrossed the Vfl33 mice with ST2- deficient mice. ST2 deficiency completely abrogated the transcriptional effects elicited by IL33 expression, suggesting that the transcriptional effects of IL33 on IEC are mediated by its mature, not its nuclear form.

Indexed as

AnimalsCell NucleusEnterocytesGene Expression RegulationInflammatory Bowel DiseasesInterleukin-1 Receptor-Like 1 ProteinInterleukin-33LymphocytesMiceMice, KnockoutIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33IL33InflammationInflammatory bowel diseaseIntestinal epithelial cellsRNA-Seq

Identifiers

PMID30145369
PMCPMC7050781
OpenAlexW2795248900

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.