Evidence map›Paper›PMID 17609265›Full record

Trial reportJournal of virology2007

Human T-cell leukemia virus type 1 (HTLV-1) p12I down-modulates ICAM-1 and -2 and reduces adherence of natural killer cells, thereby protecting HTLV-1-infected primary CD4+ T cells from autologous natural killer cell-mediated cytotoxicity despite the reduction of major histocompatibility complex class I molecules on infected cells.

Prabal Banerjee, Gerold Feuer, Edward Barker

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

49 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The role of NK cells in fighting the virus infection and sepsis.International journal of medical sciences · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

Prabal BanerjeeDepartment of Immunology and Microbiology, Rush University Medical Center, 1735 West Harrison Street, Chicago, IL 60612, USA.
Gerold Feuer
Edward Barker
SUNY Upstate Medical University · USRush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although natural killer (NK) cell-mediated control of viral infections is well documented, very little is known about the ability of NK cells to restrain human T-cell leukemia virus type 1 (HTLV-1) infection. In the current study we show that NK cells are unable to kill HTLV-1-infected primary CD4+ T cells. Exposure of NK cells to interleukin-2 (IL-2) resulted in only a marginal increase in their ability to kill HTLV-1-infected primary CD4+ T cells. This inability of NK cells to kill HTLV-1-infected CD4+ T cells occurred despite the down-modulation of major histocompatibility complex (MHC) class I molecules, one of the ligands for the major NK cell inhibitory receptor, by HTLV-1 p12(I) on CD4+ T cells. One reason for this diminished ability of NK cells to kill HTLV-1-infected cells was the decreased ability of NK cells to adhere to HTLV-1-infected cells because of HTLV-1 p12(I)-mediated down-modulation of intercellular adhesion molecule 1 (ICAM-1) and ICAM-2. We also found that HTLV-1-infected CD4+ T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell coactivating receptors, NTB-A and 2B4. Thus, despite HTLV-1-mediated down-modulation of MHC-I molecules, HTLV-1-infected primary CD4+ T cells avoids NK cell destruction by modulating ICAM expression and shunning the expression of ligands for activating receptors.

Indexed as

Antigens, CDCD4-Positive T-LymphocytesCell AdhesionCell Adhesion MoleculesCell LineCoculture TechniquesDown-RegulationHistocompatibility Antigens Class IHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Immunity, CellularIntercellular Adhesion Molecule-1Interleukin-2Killer Cells, NaturalLigandsAntigens, CDCD244 protein, humanCell Adhesion MoleculesHistocompatibility Antigens Class IICAM2 protein, humanIL2 protein, humanIntercellular Adhesion Molecule-1Interleukin-2KLRK1 protein, humanLigandsMembrane GlycoproteinsNK Cell Lectin-Like Receptor Subfamily KOncogene Proteins, Viralp12I protein, Human T-lymphotropic virus 1Receptors, Cell SurfaceReceptors, ImmunologicReceptors, Natural Killer CellSignaling Lymphocytic Activation Molecule FamilySignaling Lymphocytic Activation Molecule Family Member 1SLAMF6 protein, humanTranscription FactorsViral Regulatory and Accessory Proteins

Identifiers

PMID17609265
PMCPMC2045425
OpenAlexW2130212947

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.