Evidence map›Paper›PMID 25821356›Full record

ReviewMediators of inflammation2015

The role of innate immunity receptors in the pathogenesis of inflammatory bowel disease.

Paula Peruzzi Elia, Yolanda Faia M Tolentino, Claudio Bernardazzi, Heitor Siffert Pereira de Souza

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Veterinary sciences · 2025
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  6. Review
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  8. Review
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  15. Frontiers in veterinary science · 2020
    Article
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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.

Paula Peruzzi EliaServiço de Gastroenterologia and Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, 21941-913 Rio de Janeiro, RJ, Brazil.
Yolanda Faia M TolentinoServiço de Gastroenterologia and Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, 21941-913 Rio de Janeiro, RJ, Brazil.
Claudio BernardazziServiço de Gastroenterologia and Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, 21941-913 Rio de Janeiro, RJ, Brazil.ORCID 0000-0003-4774-902X
Heitor Siffert Pereira de SouzaServiço de Gastroenterologia and Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, 21941-913 Rio de Janeiro, RJ, Brazil ; D'Or Institute for Research and Education (IDOR), Rua Diniz Cordeiro 30, Botafogo, 22281-100 Rio de Janeiro, RJ, Brazil.
Universidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immunity constitutes the first line of defense, fundamental for the recognition and the initiation of an inflammatory response against microorganisms. The innate immune response relies on the sensing of microbial-associated molecular patterns through specialized structures such as toll-like receptors (TLRs) and the nucleotide oligomerization domain- (NOD-) like receptors (NLRs). In the gut, these tasks are performed by the epithelial barrier and the presence of adaptive and innate immune mechanisms. TLRs and NLRs are distributed throughout the gastrointestinal mucosa, being more expressed in the epithelium, and in lamina propria immune and nonimmune cells. These innate immunity receptors exhibit complementary biological functions, with evidence for pathways overlapping. However, as tolerance is the predominant physiological response in the gastrointestinal mucosa, it appears that the TLRs are relatively downregulated, while NLRs play a critical role in mucosal defense in the gut. Over the past two decades, genetic polymorphisms have been associated with several diseases including inflammatory bowel disease. Special emphasis has been given to the susceptibility to Crohn's disease, in association with abnormalities in the NOD2 and in the NLRP3/inflammasome. Nevertheless, the mechanisms underlying innate immune receptors dysfunction that result in the persistent inflammation in inflammatory bowel disease remain to be clarified.

Indexed as

AnimalsEpitheliumHumansImmunity, InnateInflammasomesInflammationInflammatory Bowel DiseasesIntestinal MucosaPolymorphism, GeneticSignal TransductionToll-Like ReceptorsInflammasomesToll-Like Receptors

Identifiers

PMID25821356
PMCPMC4364059
OpenAlexW2055005470

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.