Evidence map›Paper›PMID 27040357›Full record

ArticleImmunology2016

Endogenous TWEAK is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss.

Xuefeng Qi, Mingzhu Lei, Lijuan Qin, Mengjie Xie, Dandan Zhao, Jingyu Wang

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2016. 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
1.1field-weighted citation impact, top 24% 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, 27 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Innate Lymphoid Cells at the Maternal-Fetal Interface in Human Pregnancy.International journal of biological sciences · 2020
    Review
  13. Article
  14. Innate lymphoid cell sensing of tissue vitality.Current opinion in immunology · 2019
    Review
  15. Article
  16. Article
  17. 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

6 authors.

Xuefeng QiCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.
Mingzhu LeiCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.
Lijuan QinCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.
Mengjie XieCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.
Dandan ZhaoCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.
Jingyu WangCollege of Veterinary Medicine of Northwest A&F University, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uterine natural killer (uNK) cells are the most abundant lymphocyte population in the feto-maternal interface during early gestation, and uNK cells play a significant role in the establishment and maintenance of pregnancy-related vascularization, as well as in tolerance to the fetus. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor-inducible molecule (Fn14), are involved in preventing local cytotoxicity and counterbalancing the cytotoxic function of uNK cells. Here, we studied the regulation of TWEAK/Fn14-mediated innate immunity in the uterus using a lipopolysaccharide (LPS)-induced model of abortion in pregnant mice. Specifically, we detected the expression of TWEAK and Fn14 in the uterus and in uNK cells following LPS treatment. Our results revealed that TWEAK and Fn14 are expressed by uNK cells in pregnant mice; in particular, it appears that the cytokine TWEAK is primarily derived from uNK cells. Interestingly, the down-regulation of TWEAK in uNK cells and the up-regulation of the Fn14 receptor in the uterus in LPS-treated mice may contribute to the disruption of decidual homeostasis by altering uNK cell cytotoxicity - ultimately leading to fetal rejection. In conclusion, the present study strongly suggests that the TWEAK-Fn14 axis in uNK cells is involved in maintaining the tolerance necessary for successful pregnancy.

Indexed as

Abortion, SpontaneousAnimalsCytokine TWEAKDisease Models, AnimalFemaleKiller Cells, NaturalLipopolysaccharidesMaleMiceMice, Inbred BALB CNK Cell Lectin-Like Receptor Subfamily KPregnancyReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaTumor Necrosis FactorsTWEAK ReceptorCytokine TWEAKLipopolysaccharidesNK Cell Lectin-Like Receptor Subfamily KReceptors, Tumor Necrosis FactorTnfrsf12a protein, mouseTnfsf12 protein, mouseTumor Necrosis Factor-alphaTumor Necrosis FactorsTWEAK Receptorfibroblast growth factor-inducible moleculelipopolysaccharide-induced abortionpregnant micetumour necrosis factor-like weak inducer of apoptosisuterine natural killer cell cytotoxicity

Identifiers

PMID27040357
PMCPMC4819140
OpenAlexW2306575399

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.