Evidence map›Paper›PMID 29664401›Full record

ArticleeLife2018

Histone Deacetylase 7 mediates tissue-specific autoimmunity via control of innate effector function in invariant Natural Killer T Cells.

Herbert G Kasler, Intelly S Lee, Hyung W Lim, Eric Verdin

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Role of Histone Deacetylases in T-Cell Development and Function.International journal of molecular sciences · 2022
    Review
  7. Signals for antigen-independent differentiation of memory CD8Cellular and molecular life sciences : CMLS · 2021
    Review
  8. Article
  9. The histone methyltransferase DOT1L prevents antigen-independent differentiation and safeguards epigenetic identity of CD8Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Article
  12. Histone deacetylase function in CD4Nature reviews. Immunology · 2018
    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

4 authors at 1 institution in 1 country.

Herbert G Kasler *Gladstone Institute of Virology and Immunology, San Francisco, United States.ORCID http://orcid.org/0000-0002-6660-4267
Intelly S Lee *Gladstone Institute of Virology and Immunology, San Francisco, United States.
Hyung W LimGladstone Institute of Virology and Immunology, San Francisco, United States.
Eric VerdinGladstone Institute of Virology and Immunology, San Francisco, United States.ORCID http://orcid.org/0000-0003-3703-3183
Gladstone Institutes · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
Molecular Mechanisms of HIV LatencyR01DA041742 · NIDA · J. DAVID GLADSTONE INSTITUTES · PI VERDIN, ERIC M. · 2016 to 2021
$6.5M
Identification of HIV latency biomarkers with a dual fluorescence reporter HIVR01AI117864 · NIAID · J. DAVID GLADSTONE INSTITUTES · PI VERDIN, ERIC M. · 2015 to 2020
$3.5M
NIAID NIH HHS R01 AI117864NIDA NIH HHS R01 DA041742NIGMS NIH HHS T32 GM007618NIH HHS AI117864NIH HHS DA041742
6 · The paper itself

Abstract

We report that Histone Deacetylase 7 (HDAC7) controls the thymic effector programming of Natural Killer T (NKT) cells, and that interference with this function contributes to tissue-specific autoimmunity. Gain of HDAC7 function in thymocytes blocks both negative selection and NKT development, and diverts Vα14/Jα18 TCR transgenic thymocytes into a Tconv-like lineage. Conversely, HDAC7 deletion promotes thymocyte apoptosis and causes expansion of innate-effector cells. Investigating the mechanisms involved, we found that HDAC7 binds PLZF and modulates PLZF-dependent transcription. Moreover, HDAC7 and many of its transcriptional targets are human risk loci for IBD and PSC, autoimmune diseases that strikingly resemble the disease we observe in HDAC7 gain-of-function in mice. Importantly, reconstitution of iNKT cells in these mice mitigated their disease, suggesting that the combined defects in negative selection and iNKT cells due to altered HDAC7 function can cause tissue-restricted autoimmunity, a finding that may explain the association between HDAC7 and hepatobiliary autoimmunity.

Indexed as

AutoimmunityAnimalsAnimals, Genetically ModifiedGene DeletionGene ExpressionHistone DeacetylasesHumansMiceNatural Killer T-CellsPromyelocytic Leukemia Zinc Finger ProteinHDAC7 protein, humanHistone DeacetylasesPromyelocytic Leukemia Zinc Finger Proteinautoimmunityepigeneticsgene expressionHDAC7immunologyinflammationmouseNKT cell

Identifiers

PMID29664401
PMCPMC5943034
OpenAlexW2767150194

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.