Evidence map›Paper›PMID 35413989›Full record

ArticleVirology journal2022

Increased expression of TIGIT and KLRG1 correlates with impaired CD56

You Nie, Dandan Liu, Wen Yang, Yazhuo Li, Lihua Zhang, Xia Cheng, Ruyu Chen, Bingbing Yuan, Guangzheng Zhang, Hongwei Wang

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. NK cells in HPV-related tumorigenesis: mechanisms and clinical applications.Frontiers in cellular and infection microbiology · 2025
    Review
  8. Article
  9. NK-cell receptor modulation in viral infections.Clinical and experimental immunology · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. 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

10 authors at 1 institution in 1 country.

You Nie *Department of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Dandan Liu *Department of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Wen Yang *Department of Gynaecology and Obstetrics, Chinese PLA (People's Liberation Army) General Hospital, Beijing, China.
Yazhuo LiDepartment of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Lihua ZhangDepartment of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Xia ChengDepartment of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Ruyu ChenDepartment of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China.
Bingbing YuanBasic Medicine College, Zhengzhou University, 100 Science Avenue, Henan, China.
Guangzheng ZhangBasic Medicine College, Zhengzhou University, 100 Science Avenue, Henan, China. zgz@zzu.edu.cn.
Hongwei WangDepartment of Pathology, Fourth Medical Centre of Chinese PLA (People's Liberation Army) General Hospital, 51 Fucheng Road, Beijing, China. whw6626@sina.com.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe onset and progression of cervical intraepithelial neoplasia (CIN) are closely associated with the persistent infection of high-risk HPV (especially type16), which is mainly caused by immune escape. Natural killer (NK) cells play an important role against virally infected cells and tumor cells through a fine balance of signals from multiple surface receptors. Overexpression of non-MHC-I specific inhibitory receptors TIGIT, KLRG1, Siglec-7, LAIR-1, and CD300a on NK cells correlates with cellular exhaustion and immune evasion, but these receptors have not been investigated in CIN. The aim of the present study was to examine the potential role of NK cell non-MHC-I specific inhibitory receptors expression in immune escape from HPV16(+)CIN patients.

methodsThe subset distribution, IFN-γ and TNF-α expression levels and immunophenotype of TIGIT, KLRG1, Siglec-7, LAIR-1, and CD300a of NK cells were investigated in peripheral blood mononuclear cell samples by flow cytometry from 82 women who were HPV16(+) with CIN grades 0, I, II-III or HPV(-) CIN 0. Immunohistochemistry was applied to detect the expression of ligands for NK receptors in the cervical tissues. HPV types were identified by PCR assays.

resultsThe HPV16(+) subjects with high-grade lesions had an increased number of circulating peripheral blood CD56

conclusionsOur results suggest that up-regulation of the inhibitory TIGIT, KLRG1 and their ligands may negatively regulate cervical CD56

Indexed as

Papillomavirus InfectionsUterine Cervical DysplasiaUterine Cervical NeoplasmsFemaleHuman papillomavirus 16HumansKiller Cells, NaturalLectins, C-TypeLeukocytes, MononuclearLigandsReceptors, ImmunologicSialic Acid Binding Immunoglobulin-like LectinsKLRG1 protein, humanLectins, C-TypeLigandsReceptors, ImmunologicSialic Acid Binding Immunoglobulin-like LectinsTIGIT protein, humanCervical intraepithelial neoplasiaCytokinesHuman papillomavirus 16KLRG1-CadherinNatural killer cellTIGIT-PVR

Identifiers

PMID35413989
PMCPMC9003970
OpenAlexW4223524877

What OpenQuestion holds

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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.