Evidence map›Paper›PMID 31270148›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2019

Identification of the E3 Ligase TRIM29 as a Critical Checkpoint Regulator of NK Cell Functions.

Yaling Dou, Junji Xing, Gangcheng Kong, Guangchuan Wang, Xiaohua Lou, Xiang Xiao, Eric Vivier, Xian C Li, Zhiqiang Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 44 citations in OpenAlex.

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  4. TRIM family proteins: dual roles in tumor immunity.Frontiers in cell and developmental biology · 2026
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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

9 authors at 3 institutions in 2 countries.

Yaling DouImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.
Junji XingImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.ORCID 0000-0002-3392-5427
Gangcheng KongImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.
Guangchuan WangImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.
Xiaohua LouImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.
Xiang XiaoImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030.
Eric VivierInnate Pharma Research Labs, Innate Pharma, 13276 Marseille, France; and.ORCID 0000-0001-7022-8287
Xian C LiImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030; xcli@houstonmethodist.org zzhang@houstonmethodist.org.ORCID 0000-0002-5981-2762
Zhiqiang ZhangImmunobiology and Transplant Science Center, Houston Methodist Hospital, Houston, TX 77030; xcli@houstonmethodist.org zzhang@houstonmethodist.org.ORCID 0000-0003-1796-081X
Methodist Hospital · USCornell University · USInnate Pharma (France) · FR

Funding

Modulation of innate immune cells to create transplant toleranceR01AI080779 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI Xian Chang Li · 2011 to 2026
$5.2M
NIAID NIH HHS R01 AI080779
6 · The paper itself

Abstract

NK cells play an important role in immune surveillance and protective immunity, mainly through rapid cytokine release and cytolytic activities. But how such responses are negatively regulated remains poorly defined. In this study, we demonstrated that the E3 ubiquitin ligase TRIM29 is a crucial regulator of NK cell functions. We found that TRIM29 was not expressed in resting NK cells, but was readily upregulated following activation, especially after IL-12 plus IL-18 stimulation. The levels of TRIM29 expression were inversely correlated with IFN-γ production by NK cells, suggesting that TRIM29 inhibits NK cell functions. Indeed, deficiency of TRIM29, specifically in NK cells, resulted in an enhanced IFN-γ production and consequently protected mice from murine CMV infection. Mechanistically, we showed that once induced in NK cells, TRIM29 ubiquitinates and degrades the TGF-β-activated kinase 1 binding protein 2 (TAB2), a key adaptor protein in IFN-γ production by NK cells. These results identify TRIM29 as a negative regulator of NK cell functions and may have important clinical implications.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsKiller Cells, NaturalLymphocyte ActivationMiceTranscription FactorsUbiquitinationAdaptor Proteins, Signal TransducingTab2 protein, mouseTranscription FactorsTRIM29 protein, mouse

Identifiers

PMID31270148
PMCPMC6684831
OpenAlexW2955513834

What OpenQuestion holds

Textmetadata
LicenceTDM
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.