Evidence map›Paper›PMID 27183588›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Nod1 Limits Colitis-Associated Tumorigenesis by Regulating IFN-γ Production.

Yu Zhan, Sergey S Seregin, Jiachen Chen, Grace Y Chen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024
    Review
  4. Article
  5. NOD1: a metabolic modulator.Frontiers in endocrinology · 2024
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Significance and Role of Pattern Recognition Receptors in Malignancy.Archivum immunologiae et therapiae experimentalis · 2019
    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.

Yu ZhanDivision of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109.
Sergey S SereginDivision of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-9241-4555
Jiachen ChenDivision of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109.
Grace Y ChenDivision of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109 gchenry@umich.edu.ORCID 0000-0001-6434-8696
University of Michigan · US

Funding

Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
Regulation of intestinal inflammation and tumorigenesis by Nlrp6R01CA166879 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, GRACE Y. · 2013 to 2017
$1.6M
Understanding Nlrp6 function in inflammatory monocytes during inflammation and tumorigenesisF32CA200144 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEREGIN, SERGEY S · 2015 to 2016
$117k
NCATS NIH HHS UL1 TR000433NCI NIH HHS F32 CA200144NCI NIH HHS R01 CA166879
6 · The paper itself

Abstract

Chronic intestinal inflammation is a major risk factor for the development of colorectal cancer. Nod1, a member of the Nod-like receptor (NLR) family of pattern recognition receptors, is a bacterial sensor that has been previously demonstrated to reduce susceptibility of mice to chemically induced colitis and subsequent tumorigenesis, but the mechanism by which it mediates its protection has not been elucidated. In this study, we show that Nod1 expression in the hematopoietic cell compartment is critical for limiting inflammation-induced intestinal tumorigenesis. Specifically, Nod1-deficient T cells exhibit impaired IFN-γ production during dextran sulfate sodium (DSS)-induced acute inflammation in vivo, and administration of the Nod1 ligand KF1B enhances IFN-γ responses by anti-CD3-activated T cells in vitro. Absence of IFN-γ signaling results in increased inflammation-associated tumors in mice, and adoptive transfer of Nod1(-/-) or IFNγ(-/-) T cells into T cell-deficient mice results in increased tumorigenesis as compared with T cell-deficient mice that were adoptively transferred with wild-type T cells. Collectively, these results suggest a previously unappreciated role for the innate immune receptor Nod1 in suppressing colitis-associated tumorigenesis through a T cell-mediated mechanism.

Indexed as

CarcinogenesisGene Expression RegulationAdoptive TransferAnimalsColitisDextran SulfateDisease Models, AnimalImmunity, InnateInflammationInterferon-gammaIntestinesMiceMice, Inbred C57BLMice, KnockoutNod1 Signaling Adaptor ProteinT-LymphocytesDextran SulfateInterferon-gammaNod1 protein, mouseNod1 Signaling Adaptor Protein

Identifiers

PMID27183588
PMCPMC4893968
OpenAlexW2345736093

What OpenQuestion holds

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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.