Evidence map›Paper›PMID 29731749›Full record

ArticleFrontiers in immunology2018

Adaptive NKG2C

Hassen Kared, Serena Martelli, Shu Wen Tan, Yannick Simoni, Meng Li Chong, Siew Hwei Yap, Evan W Newell, Sylvia L F Pender, Adeeba Kamarulzaman, Reena Rajasuriar and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. TIM-3, a potential target for sepsis therapy.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
    Review
  4. Article
  5. Resident CD49aScience advances · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. OMIP-098: A 26 parameter, 24 color flow cytometry panel for human memory NK cell phenotyping.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors.

Hassen KaredSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.
Serena MartelliSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.
Shu Wen TanSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.
Yannick SimoniSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.
Meng Li ChongCentre of Excellence for Research in AIDS (CERiA), University of Malaya, Kuala Lumpur, Malaysia.
Siew Hwei YapCentre of Excellence for Research in AIDS (CERiA), University of Malaya, Kuala Lumpur, Malaysia.
Evan W NewellSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.
Sylvia L F PenderAcademic Unit of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Adeeba KamarulzamanCentre of Excellence for Research in AIDS (CERiA), University of Malaya, Kuala Lumpur, Malaysia.
Reena RajasuriarCentre of Excellence for Research in AIDS (CERiA), University of Malaya, Kuala Lumpur, Malaysia.
Anis LarbiSingapore Immunology Network (SIgN), Aging and Immunity Program, Agency for Science Technology and Research (ASTAR), Singapore, Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Repetitive stimulation by persistent pathogens such as human cytomegalovirus (HCMV) or human immunodeficiency virus (HIV) induces the differentiation of natural killer (NK) cells. This maturation pathway is characterized by the acquisition of phenotypic markers, CD2, CD57, and NKG2C, and effector functions-a process regulated by Tim-3 and orchestrated by a complex network of transcriptional factors, involving T-bet, Eomes, Zeb2, promyelocytic leukemia zinc finger protein, and Foxo3. Here, we show that persistent immune activation during chronic viral co-infections (HCMV, hepatitis C virus, and HIV) interferes with the functional phenotype of NK cells by modulating the Tim-3 pathway; a decrease in Tim-3 expression combined with the acquisition of inhibitory receptors skewed NK cells toward an exhausted and cytotoxic phenotype in an inflammatory environment during chronic HIV infection. A better understanding of the mechanisms underlying NK cell differentiation could aid the identification of new immunological targets for checkpoint blockade therapies in a manner that is relevant to chronic infection and cancer.

Indexed as

CD57 AntigensCoinfectionCytomegalovirus InfectionsHepatitis A Virus Cellular Receptor 2Hepatitis CHIV InfectionsHumansKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily CCD57 AntigensHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2KLRC2 protein, humanNK Cell Lectin-Like Receptor Subfamily Cagingcancercheckpoint blockadechronic infectionexhaustionmaturationnatural killer cellssenescence

Identifiers

PMID29731749
PMCPMC5919961

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.