Evidence map›Paper›PMID 28322135›Full record

ReviewCritical reviews in immunology2016

The Goldilocks Conundrum: NLR Inflammasome Modulation of Gastrointestinal Inflammation during Inflammatory Bowel Disease.

Veronica M Ringel-Scaia, Dylan K McDaniel, Irving C Allen

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Pyroptosis-Induced Inflammation and Tissue Damage.Journal of molecular biology · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Interleukin-18 binding protein attenuates renal injury of adriamycin-induced mouse nephropathy.International journal of clinical and experimental pathology · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. 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

3 authors at 2 institutions in 1 country.

Veronica M Ringel-ScaiaGraduate Program in Translational Biology, Medicine, and Health, Virginia Tech, Blacksburg, VA 24061.
Dylan K McDanielDepartment of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Irving C AllenGraduate Program in Translational Biology, Medicine, and Health, Virginia Tech, Blacksburg, VA 24061; Department of Biomedical Sciences and Pathobiology, Virginia Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061.
Virginia–Maryland College of Veterinary Medicine · USVirginia Tech · US

Funding

NLR Regulation of Gastrointestinal Inflammation and TumorigenesisK01DK092355 · NIDDK · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI ALLEN, IRVING C · 2011 to 2015
$709k
Evaluating NLR Modulation of Canonical and Non-Canonical NF-kB Signaling in IBDR03DK105975 · NIDDK · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI ALLEN, IRVING C · 2015 to 2016
$161k
NIDDK NIH HHS K01 DK092355NIDDK NIH HHS R03 DK105975
6 · The paper itself

Abstract

Recent advances have revealed significant insight into inflammatory bowel disease (IBD) pathobiology. Ulcerative colitis and Crohn's disease, the chronic relapsing clinical manifestations of IBD, are complex disorders with genetic and environmental influences. These diseases are associated with the dysregulation of immune tolerance, excessive inflammation, and damage to the epithelial cell barrier. Increasing evidence indicates that pattern recognition receptors, including Toll-like receptors (TLRs) and nucleotide-binding domain and leucine-rich repeat-containing proteins (NLRs), function to maintain immune system homeostasis, modulate the gastrointestinal microbiome, and promote proper intestinal epithelial cell regeneration and repair. New insights have revealed that NLR family members are essential components in maintaining this immune system homeostasis. To date, the vast majority of studies associated with NLRs have focused on family members that form a multiprotein signaling platform called the inflammasome. These signaling complexes are responsible for the cleavage and activation of the potent pleotropic cytokines IL-1β and IL-18, and they facilitate a unique form of cell death defined as pyroptosis. In this review, we summarize the current paradigms associated with NLR inflammasome maintenance of immune system homeostasis in the gastrointestinal system. New concepts related to canonical and noncanonical inflammasome signaling, as well as the implications of classical and alternative inflammasomes in IBD pathogenesis, are also reviewed.

Indexed as

AnimalsGastrointestinal MicrobiomeHumansImmune SystemInflammasomesInflammatory Bowel DiseasesLeucine-Rich Repeat ProteinsNeoplasmsNLR ProteinsProteinsSignal TransductionToll-Like ReceptorsInflammasomesLeucine-Rich Repeat ProteinsNLR ProteinsProteinsToll-Like Receptors

Identifiers

PMID28322135
PMCPMC5364818
OpenAlexW2570123109

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.