Evidence map›Paper›PMID 21687547›Full record

ArticleJournal of biomedicine & biotechnology2011

Potential role of NK cells in the pathogenesis of inflammatory bowel disease.

Praveen K Yadav, Chi Chen, Zhanju Liu

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Recent Advances in Cell-Based In Vitro Models to Recreate Human Intestinal Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. IBD therapeutics: what is in the pipeline?Frontline gastroenterology · 2022
    Article
  15. Review
  16. Article
  17. NKp46+ lamina propria natural killer cells undergo metabolic reprogramming in a mouse experimental colitis model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Praveen K YadavDepartment of Gastroenterology, The Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Chi Chen
Zhanju Liu
Tongji University · CNShanghai Tenth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NK cells are a major component of the innate immune system and play an important role in the tissue inflammation associated with autoimmune diseases such as inflammatory bowel disease (IBD). NK cells are unique in bearing both stimulatory and inhibitory receptors specific for MHC class I molecules, and their function is regulated by a series of inhibiting or activating signals. The delicate balance between activation and inhibition that decides NK cell final action provides an opportunity for their possible modulatory effect on specific therapeutic settings. Intestinal NK cells are phenotypically distinct from their counterparts in the blood and resemble "helper" NK cells, which have potentially important functions both in promoting antipathogen responses and in the maintenance of intestinal epithelial homeostasis. NK cell activities have been found to be significantly below normal levels in both remissive and active stages of IBD patients. However, some proinflammatory cytokines (e.g., IL-15, IL-21, and IL-23) could potently induce NK cell activation to secret high levels of proinflammatory cytokines (e.g., IFN-γ and TNF) and promote the cytolytic activities against the target cells. This paper provides the characteristics of intestinal NK cells and their potential role in the pathogenesis of IBD.

Indexed as

Autoimmune DiseasesCytokinesHistocompatibility Antigens Class IHumansImmunity, InnateInflammatory Bowel DiseasesInterleukin-15Interleukin-21Interleukin-23InterleukinsIntestinal MucosaKiller Cells, NaturalLymphocyte ActivationT-Lymphocytes, Helper-InducerCytokinesHistocompatibility Antigens Class IInterleukin-15Interleukin-21Interleukin-23Interleukins

Identifiers

PMID21687547
PMCPMC3114561
OpenAlexW1973009696

What OpenQuestion holds

Textmetadata
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.