Evidence map›Paper›PMID 22508835›Full record

ArticleThe Journal of experimental medicine2012

Human invariant natural killer T cells acquire transient innate responsiveness via histone H4 acetylation induced by weak TCR stimulation.

Xiaohua Wang, Kathleen A Bishop, Subramanya Hegde, Lance A Rodenkirch, J Wesley Pike, Jenny E Gumperz

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–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

34 citing papers in PubMed.

  1. Human CD4Frontiers in immunology · 2026
    Article
  2. Article
  3. Human CD4Immunology · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Article
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  11. Article
  12. Review
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  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. T Cells Going Innate.Trends in immunology · 2016
    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

6 authors.

Xiaohua WangDepartment of Medical Microbiology and Immunology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53706, USA.
Kathleen A Bishop
Subramanya Hegde
Lance A Rodenkirch
J Wesley Pike
Jenny E Gumperz

Funding

Analysis of Human NKT cell auto-antigensR01AI074940 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI GUMPERZ, JENNY E. · 2009 to 2013
$1.8M
Structural determinants of CD1d-restricted TCR functionR01AI060777 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI GUMPERZ, JENNY E. · 2004 to 2008
$1.4M
NIAID NIH HHS R01 AI060777NIAID NIH HHS R01 AI074940
6 · The paper itself

Abstract

Invariant NKT cells (iNKT cells) are innate T lymphocytes that are thought to play an important role in producing an early burst of IFN-γ that promotes successful tumor immunosurveillance and antimicrobial immunity. The cellular activation processes underlying innate IFN-γ production remain poorly understood. We show here that weak T cell receptor (TCR) stimulation that does not directly activate iNKT cell IFN-γ messenger RNA transcription nevertheless induces histone H4 acetylation at specific regions near the IFNG gene locus. This renders the iNKT cells able to produce IFN-γ in an innate manner (i.e., not requiring concurrent TCR stimulation) upon exposure to IL-12 and IL-18. The iNKT cells retain the capacity for innate activation for hours to days after the initial weak TCR stimulation, although their innate responsiveness gradually declines as a function of histone deacetylation. These results explain how iNKT cells are able to mediate rapid innate IFN-γ secretion in a manner that does not require them to undergo permanent T(H1) differentiation. Moreover, our results also indicate that iNKT cell motility is maintained during activation by IL-12 and IL-18. Therefore, iNKT cells activated through this pathway can continue to migrate and may thus disseminate the IFN-γ that they produce, which may amplify its impact.

Indexed as

AcetylationChromatin ImmunoprecipitationDNA PrimersFlow CytometryGene Expression RegulationHistonesHumansImmunity, InnateInterferon-gammaInterleukin-12Interleukin-18Microscopy, ConfocalNatural Killer T-CellsReal-Time Polymerase Chain ReactionReceptors, Antigen, T-CellReverse Transcriptase Polymerase Chain ReactionDNA PrimersHistonesInterferon-gammaInterleukin-12Interleukin-18Receptors, Antigen, T-CellRNA, MessengerSTAT4 protein, humanSTAT4 Transcription Factor

Identifiers

PMID22508835
PMCPMC3348100

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.