Evidence map›Paper›PMID 20224552›Full record

ArticleThe EMBO journal2010

Regulation of natural killer T-cell development by deubiquitinase CYLD.

Andrew J Lee, Xiaofei Zhou, Mikyoung Chang, John Hunzeker, Robert H Bonneau, Dapeng Zhou, Shao-Cong Sun

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Deubiquitinases and Cancer.Journal of pharmacy & bioallied sciences · 2024
    Review
  3. Review
  4. Interleukin (IL)-7 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Article
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  6. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Andrew J LeeDepartment of Immunology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Xiaofei Zhou
Mikyoung Chang
John Hunzeker
Robert H Bonneau
Dapeng Zhou
Shao-Cong Sun
Pennsylvania State University · USThe University of Texas MD Anderson Cancer Center · USUniversity of Houston · US

Funding

TpI2 Kinase in Macrophage Activation by MicrobesR01AI057555 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2004 to 2021
$6.7M
Molecular Studies of Noncanonical NF-kb SignalingR01GM084459 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2008 to 2021
$4.4M
Signaling Functions of the Tumor Suppressor CYLDR01AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2006 to 2014
$3.6M
Regulation of T-cell function and autoimmune inflammation by deubiquitinases.R37AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2015 to 2021
$2.8M
Endogenous glycosphingolipid antigens for NKT cellsR01AI079232 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ZHOU, DAPENG · 2009 to 2013
$1.9M
NIAID NIH HHS AI057555NIAID NIH HHS AI064639NIAID NIH HHS R01 AI057555NIAID NIH HHS R01 AI064639NIAID NIH HHS R01 AI079232NIAID NIH HHS R37 AI064639NIGMS NIH HHS GM084459NIGMS NIH HHS R01 GM084459
6 · The paper itself

Abstract

Natural killer T (NKT) cells modulate immune responses against pathogens and tumours, as well as immunological tolerance. We show here that CYLD, a tumour suppressor with deubiquitinase function, has a pivotal and cell-intrinsic function in NKT cell development. Unlike other known NKT regulators, CYLD is dispensable for intrathymic NKT cell maturation but is obligatory for the survival of immature NKT cells. Interestingly, CYLD deficiency impairs the expression of ICOS, a costimulatory molecule required for the survival and homeostasis of NKT cells, and this molecular defect is associated with attenuated response to an NKT-survival cytokine, IL-7, due to reduced expression of IL-7 receptor. We show, for the first time, that IL-7 induces the expression of ICOS in NKT cells, which is largely dependent on CYLD. Interestingly, loss of CYLD causes constitutive NF-kappaB activation in developing NKT cells, which contributes to their defective IL-7 response and attenuated ICOS expression. These findings establish CYLD as a critical regulator of NKT cell development and provide molecular insights into this novel function of CYLD.

Indexed as

LymphopoiesisAnimalsAntigens, Differentiation, T-LymphocyteApoptosisCysteine EndopeptidasesDeubiquitinating Enzyme CYLDInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinInterleukin-7MiceMice, Inbred C57BLMice, KnockoutNatural Killer T-CellsNF-kappa BPhenotypeProteinsAntigens, Differentiation, T-LymphocyteCYLD protein, mouseCysteine EndopeptidasesDeubiquitinating Enzyme CYLDIcosl protein, mouseIcos protein, mouseInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinInterleukin-7NF-kappa BProteinsReceptors, Interleukin-7

Identifiers

PMID20224552
PMCPMC2876956
OpenAlexW2094791901

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.